Freie Radikale & Oxidativer Stress
Aktuelle wissenschaftliche Studien | 61-80
61: Curr Opin Obstet Gynecol. 2006 Jun;18(3):325-32.
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The role of free radicals and antioxidants in reproduction.
Agarwal A, Gupta S, Sikka S.
Center for Advanced Research in Human Reproduction, Infertility and Sexual Function, Glickman Urological Institute and the Department of Obstetrics-Gynecology, Cleveland Clinic, Cleveland, Ohio 44195, USA. Agarwaa@ccf.org
PURPOSE OF REVIEW: This review summarizes the role of free radicals and oxidative stress in the pathophysiology of human reproduction. RECENT FINDINGS: An extensive review of the literature on the role of oxidative stress in influencing assisted reproduction and its outcome is described in this article. Free radicals or reactive oxygen species mediate their action through many of the proinflammatory cytokines and this mechanism has been proposed as a common underlying factor for endometriosis, ovarian cancer, polycystic ovary disease, and various other pathologies affecting the female reproductive process, as highlighted in this review. Oxidative stress, sperm DNA damage, and apoptosis have been implicated in male infertility. Elevated reactive oxygen species levels correlate with the poor fertility outcomes seen in the assisted reproductive technology setting. SUMMARY: Oxidative stress has been implicated in male and female infertility, including fetal dysmorphogenesis, abortions, and intrauterine growth restriction. Accurate evaluation of seminal oxidative stress by standardized assays may help in the diagnosis and management of male infertility. There is evidence in the literature on the beneficial effects of oral antioxidant supplementation in male infertility. Current ongoing trials will provide answers on the safety and effectiveness of antioxidants in improving maternal and fetal outcomes. Further studies need to be conducted to determine if antioxidant supplementation will prevent fetal developmental defects in high-risk pregnancy with diabetes.
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PMID: 16735834 [PubMed - indexed for MEDLINE]
62: Hepatology. 2006 Jun;43(6):1248-56.
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Renal damage in experimentally-induced cirrhosis in rats: Role of oxygen free radicals.
Natarajan SK, Basivireddy J, Ramachandran A, Thomas S, Ramamoorthy P, Pulimood AB, Jacob M, Balasubramanian KA.
Wellcome Trust Research Laboratory, Department of Gastrointestinal Sciences, Christian Medical College, Vellore, India.
Cirrhosis with ascites is associated with impaired renal function accompanied by sodium and water retention. Although it has been suggested that mediators such as nitric oxide play a role in the development of renal failure in this situation, other mechanisms underlying the process are not well understood. This study examined the role of oxidative stress in mediating renal damage during the development of cirrhosis in order to understand mechanisms involved in the process. It was shown that carbon tetrachloride- or thioacetamide-induced cirrhosis in rats results in oxidative stress in the kidney as seen by increased lipid peroxidation and protein oxidation, accompanied by altered antioxidant status. Cirrhosis was also found to affect renal mitochondrial function, as assessed by measurement of the respiratory control ratio, the swelling of mitochondria, and calcium flux across mitochondrial membranes. Increased lipid peroxidation and changes in lipid composition were evident in the renal brush border membranes, with compromised transport of 14C glucose across these membranes. In conclusion, renal alterations produced as a result of cirrhosis in the rat are possibly mediated by oxidative stress.
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PMID: 16729302 [PubMed - indexed for MEDLINE]
63: J Perinat Neonatal Nurs. 2006 Apr-Jun;20(2):125-7.
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Free radicals in perinatal and neonatal care, part 2: oxidative stress during the perinatal and neonatal period.
Blackburn S.
Department of Family and Child Nursing University of Washington, Seattle, WA, USA.
Publication Types:
PMID: 16714911 [PubMed - indexed for MEDLINE]
64: Int J Oncol. 2006 Jun;28(6):1491-505.
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Induction of DNA double-strand breaks in A549 and normal human pulmonary epithelial cells by cigarette smoke is mediated by free radicals.
Albino AP, Huang X, Jorgensen ED, Gietl D, Traganos F, Darzynkiewicz Z.
Vector Research Ltd., New York, NY 10019, USA. talbino@vectorgroupltd.com
DNA double-strand breaks (DSBs) are potentially mutagenic/carcinogenic lesions. Induction of DSBs triggers phosphorylation of histone H2AX on Ser-139. Phosphorylated H2AX (gammaH2AX) can be detected immunocytochemically, and the intensity of gammaH2AX immunofluorescence (IF), reflecting the number of gammaH2AX-IF foci per nucleus, reveals the frequency of DSBs. Using multiparameter cytometric analysis of gammaH2AX-IF, we previously observed that DSBs are induced in normal human bronchial epithelial (NHBE) and A549 pulmonary adenocarcinoma cells following exposure to cigarette smoke (CS) or smoke condensate. In the present study, we show that N-acetyl L-cysteine (NAC) and glutathione, both effective scavengers of free radicals, prevented induction of DSBs by CS in these cells. In contrast, the glutathione synthesis inhibitor, DL-Buthionine-[S,R]-sulfoximine (BSO), enhanced the induction of DSBs by CS. The observed reduction of DSBs by NAC correlated with protection of the reproductive capability (clonogenicity) of A549 cells treated with CS. The data implicate formation of free radicals by CS as factors generating DSBs and affecting cell survival. Interestingly, at the conditions of exposure to CS when clonogenicity was only moderately affected, S-phase cells showed significantly higher sensitivity in terms of induction of DSBs compared with G1 or G2M cells. In light of the evidence that CS increases oxidative stress and induces cell proliferation in the lungs of smokers, the high propensity of S-phase cells to develop DSBs upon exposure to CS has to be considered as a potentially pathogenic event in smoke-induced tumor development. This is the first report to reveal cell cycle-phase specificity in both the induction of DSBs by CS and their prevention by free radical scavengers. The detection of gammaH2AX to assess the induction of CS-induced DSBs and their relationship to cell cycle phase provides a convenient tool to explore approaches to protect cells from this type of genotoxic damage.
PMID: 16685450 [PubMed - indexed for MEDLINE]
65: Ann Clin Lab Sci. 2006 Spring;36(2):174-8.
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Effects of diabetes duration and glycemic control on free radicals in children with type 1 diabetes mellitus.
Hsu WT, Tsai LY, Lin SK, Hsiao JK, Chen BH.
Department of Laboratory Medicine, Kaohsiung Medical University, Chung-Ho Memorial Hospital, No. 100, Shih Chuan 1st Road, Kaohsiung 807, Taiwan.
Parameters of lipid peroxidation, protein oxidation, and antioxidant defense systems were measured in blood samples from 47 children with type 1 diabetes mellitus and from 51 healthy controls, matched for age and sex. In the diabetic children, chemiluminescent assay of plasma superoxide anion gave photoemission (counts x 10(3), mean +/- SD) of 674 +/- 412, which were significantly higher than those in the controls (452 +/- 185; p <0.05). Plasma vitamin A levels in the diabetic children (243 +/- 90 microg/dl) were also higher than those in the controls (207 +/- 59 microg/dl, p <0.05). In a subgroup of 24 diabetic children with blood HbA1C levels >or=8.5%, plasma lipoperoxide (LPO) and vitamin E levels were higher (p <0.05) than those in 23 diabetic children with blood HbA1C levels <8.5%. In a subgroup of 26 children with diabetes duration >or=5 yr, plasma LPO levels were higher (p <0.05) than those in 21 children with diabetes duration <5 yr. These findings confirm the presence of oxidant stress in children with type 1 diabetes mellitus and demonstrate that certain indices of oxidant stress are influenced by the duration of diabetes and by the efficacy of glycemic control. These observations suggest that supportive therapy aimed at oxidative stress may help to prevent clinical complications in children with type 1 diabetes mellitus.
PMID: 16682514 [PubMed - indexed for MEDLINE]
66: Biotechnol Bioeng. 2006 Sep 5;95(1):48-57.
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Inactivation of herpes simplex type 1 gene vector on immobilized metal affinity chromatography: oxidative damage by hydroxyl free radicals and its prevention.
Jiang C, Ataai M, Ozuer A, Krisky D, Wechuck J, Pornsuwan S, Pourarian F, Glorioso JC.
Department of Chemical Engineering, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA.
Metal catalyzed oxidation (MCO), which typically involves oxygen free radical generation, is an important pathway that leads to the deterioration of many biological molecules in solution. The occurrence of MCO in immobilized metal affinity chromatography (IMAC) systems and its potential for inactivating biological products has not been well recognized. In this study, we report the inactivation of herpes simplex virus type 1 (HSV-1) gene therapy vector on immobilized cobalt affinity chromatography. We observed that purification of KgBHAT, an HSV-1 mutant bearing cobalt affinity tags (HAT) on the surface, on an IDA-Co2+ column using crude supernatant as starting material resulted in signification loss in virus infectivity (<5% recovery). Electron spin resonance (ESR) revealed that the virus inactivation was caused by hydroxyl free radicals generated from the interactions between cellular impurities and the metal ions on the column. Inclusion of 20 mM ascorbate, a free radical scavenger, in the chromatography mobile phase effectively scavenged the hydroxyl radicals and dramatically augmented the infectivity recovery to 70%. This finding is the first demonstration of oxygen free radical-mediated biological inactivation in an actual IMAC purification and the way on how to effectively prevent it. (c) 2006 Wiley Periodicals, Inc.
Publication Types:
PMID: 16673413 [PubMed - indexed for MEDLINE]
67: Arch Oral Biol. 2006 Aug;51(8):640-8. Epub 2006 Apr 18.
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Free radicals related effects and antioxidants in saliva and serum of adolescents with Type 1 diabetes mellitus.
Reznick AZ, Shehadeh N, Shafir Y, Nagler RM.
Department of Anatomy and Cell Biology, Rambam Medical Center and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
OBJECTIVE: The purpose of the current study was to analyze both serum and salivary composition and oxidative stress markers in Type 1 diabetes mellitus (DM) patients. DESIGN: Twenty consenting patients with DM but otherwise healthy patients aged 13-19 years and 12 healthy controls, matching in age and gender (Group 1), participated in the study. The patients were divided according to those who had controlled diabetes mellitus (Group 2) or uncontrolled diabetes mellitus (Group 3). All were analyzed for saliva composition and antioxidants. Saliva was also analyzed for its levels of superoxide dismutase (SOD) and amylase activity, total IgA and total IgG concentrations and potassium, phosphorus, magnesium and calcium electrolyte concentrations. RESULTS: A significant correlation was found between the severity of the DM/HbA1c values and the increase in both salivary and/or serum antioxidants (peroxidase, SOD and TAS), and the various TCL parameters (H1, H3, pre-incubation and oxygenation-potential). CONCLUSIONS: The two most important findings of the current study relate to the role of oxidative stress in the pathogenesis of Type 1 diabetes mellitus and to the involvement of salivary glands in the disease. The profound effects of DM on salivary antioxidant parameters may be also of great importance in respect to the diagnosis and evaluation of the disease. The correlation between altered salivary parameters and the severity of the disease may indicate that evaluation of the salivary status of DM patients as part of the assessment of their disease activity and severity is warranted.
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PMID: 16620776 [PubMed - indexed for MEDLINE]
68: Biol Pharm Bull. 2006 Apr;29(4):805-10.
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Effects of amelioration of total flavonoids from stems and leaves of Scutellaria baicalensis Georgi on cognitive deficits, neuronal damage and free radicals disorder induced by cerebral ischemia in rats.
Shang YZ, Miao H, Cheng JJ, Qi JM.
Institute of Traditional Chinese Medicine, Chengde Medical College, China. shangyz1018@yahoo.com.cn
Previous studies reported that the total flavonoids from the stems and leaves of Scutellaria baicalensis Georgi (TFSS) could enhance and improve learning and memory abilities in experimental animals, and reduce the neuronal pathologic alterations induced by some reagents in mice. The present study examined whether TFSS can improve memory dysfunction, neuronal damage, and abnormal free radicals induced by permanent cerebral ischemia in rats. The permanent cerebral ischemic model in rats was produced by bilateral ligation of the common carotid arteries. The influence of permanent cerebral ischemia on learning and memory was determined in the Morris water maze. The neuronal damage in the hippocampus and cerebral cortex was assessed by the neuronal morphologic observations. The contents of malondialdehyde (MDA) and nitric oxide (NO), and the activities of superoxide dismutase (SOD) and catalase (CAT) in the hippocampus and cerebral cortex were measured using thiobarbituric acid, nitrate reductase, xanthine-xanthine oxidase, and ammonium molybdate spectrophotometric methods, respectively. In learning and memory performance tests, cerebral ischemic rats always required a longer latency time to find the hidden platform and spent a shorter time in the target quadrant in the Morris water maze. TFSS 17.5-70 mg.kg(-1) daily orally administered to ischemic rats for 20 d, from day 16-35 after operation differently reduced the prolonged latency and increased swimming time spent in the target quadrant. In neuronal morphologic observations, daily oral TFSS 17.5-70 mg.kg(-1) for 21 d, from day 16-36 after operation markedly inhibited the ischemia-induced neuronal damage. In addition, the increased contents of MDA and NO, and SOD activity, and the decreased activity of CAT in the hippocampus and cerebral cortex induced by cerebral ischemia were differently reversed. The reference drug piracetam (140 mg.kg(-1) per day for 20-21 d) similarly improved impaired memory and neuronal damage but had no significant effects on free radicals in ligated rats. TFSS can improve memory deficits and neuronal damage in rats after permanent cerebral ischemia, which may be beneficial in the treatment of cerebrovascular dementia.
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PMID: 16595923 [PubMed - indexed for MEDLINE]
69: J Cell Mol Med. 2006 Jan-Mar;10(1):206-15.
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Age-associated changes in oxidative damage and the activity of antioxidant enzymes in rats with inherited overgeneration of free radicals.
Sinitsyna O, Krysanova Z, Ishchenko A, Dikalova AE, Stolyarov S, Kolosova N, Vasunina E, Nevinsky G.
SD RAS Institute of Cytology and Genetics, 10 Lavrentieva Ave., Novosibirsk, Russia.
Reactive oxygen species have been hypothesized to play an important role in the process of aging. To investigate the correlation between oxidative stress and accumulation of protein and DNA damage, we have compared the age-dependent levels of protein carbonyl groups and the activities of antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase in cytosol and mitochondrial extracts from liver cells of Wistar and OXYS rats. The latter strain is characterized by increased sensitivity to free radicals. Faster age-dependent increase in the level of protein carbonyl groups was found in OXYS as compared with Wistar rats. A complicated enzyme-specific pattern of age-dependent changes in the activities of antioxidant enzymes was observed. Long-term uptake of dietary supplements Mirtilene forte (extract from the fruits of Vaccinium myrtillus L.) or Adrusen zinco (vitamin E complex with zinc, copper, selenium and omega-3 polyunsaturated fatty acids) sharply decreased the level of protein oxidation in cytosol and mitochondrial extracts of hepatocytes of Wistar and of OXYS rats. Both dietary supplements increased the activity of catalase in the liver mitochondria of OXYS rats. Our results are in agreement with the shorter life-span of OXYS and with the mitochondrial theory of aging, which postulates that accumulation of DNA and protein lesions leads to mitochondrial dysfunction and accelerates the process of aging.
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PMID: 16563232 [PubMed - indexed for MEDLINE]
70: Mol Microbiol. 2006 Mar;59(6):1744-53.
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5'-Adenosinephosphosulphate reductase (CysH) protects Mycobacterium tuberculosis against free radicals during chronic infection phase in mice.
Senaratne RH, De Silva AD, Williams SJ, Mougous JD, Reader JR, Zhang T, Chan S, Sidders B, Lee DH, Chan J, Bertozzi CR, Riley LW.
School of Public Health, University of California, Berkeley, 94720, USA.
A major obstacle to tuberculosis (TB) control is the problem of chronic TB infection (CTBI). Here we report that 5'-adenosinephosphosulphate reductase (CysH), an enzyme essential for the production of reduced-sulphur-containing metabolites, is critical for Mycobacterium tuberculosis (Mtb) survival in chronic infection phase in mice. Disruption of cysH rendered Mtb auxotrophic for cysteine and methionine, and attenuated virulence in BALB/c and C57BL/6 immunocompetent mice. The mutant and wild-type Mtb replicated similarly during the acute phase of infection, but the mutant showed reduced viability during the persistent phase of the infection. The cysH mutant caused disease and death after 4-7 weeks of infection in four different groups of mice - Rag1(-/-), NOS2(-/-), gp91phox(-/-) NOS2(-/-) and gp91phox(-/-) mice given aminoguanidine [to suppress the effects of nitric oxide synthase 2 (NOS2)]- indicating minimal metabolic effect on the cysH mutant survival in these mice. The cysH mutant was also susceptible to peroxynitrite and hydrogen peroxide in vitro. These results show that CysH is important for Mtb protection during the chronic infection phase, and that resistance to nitrosative and oxidative stress may be the mechanism of this protection. Thus, this metabolic gene of an intracellular pathogen could have a secondary role in protection against the host immune response. Finally the lack of an endogenous human orthologue of cysH and its possible role in defence against adaptive immunity renders CysH an attractive enzyme for further studies as a target for therapeutics active against CTBI.
PMID: 16553880 [PubMed - indexed for MEDLINE]
71: Med Sci (Paris). 2006 Mar;22(3):266-72.
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[Ageing free radicals and cellular stress]
[Article in French]
Barouki R.
Inserm UMR-S490, Université René Descartes, 45, rue des Saints Pères, 75270 Paris Cedex 06, France. robert.barouki@univ-paris5.fr
A number of theories have attempted to account for ageing processes in various species. Following the << rate of living >> theory of Pearl, Harman suggested fifty years ago that the accumulation of oxidants could explain the alteration of physical and cognitive functions with ageing. Oxygen metabolism leads to reactive species, including free radicals, which tend to oxidize surrounding molecules such as DNA, proteins and lipids. As a consequence various functions of cells and tissues can be altered, leading to DNA instability, protein denaturation and accumulation of lipid byproducts. Oxidative stress is an adaptive process which is triggered upon oxidant accumulation and which comprises the induction of protective and survival functions. Experimental evidence suggests that the ageing organism is in a state of oxidative stress, which supports the free radical theory. A number of other theories have been proposed ; some of these are actually compatible with the free radical theory. Caloric restriction is among the best models to increase life span in many species. While the relationship between caloric restriction and corrected metabolic rate is controversial, the decrease in ROS production by mitochondria appears to be experimentally supported. The ROS and mitochondrial theories of ageing appear to be compatible. Genetic models of increased life span, particularly those affecting the Foxo pathway, are usually accompanied by an increased resistance to oxidative insult. The free radical theory is not consistent with programmed senescence theories involving the cell division dependent decrease in telomere length ; however, oxidants are known to alter telomere structure. An appealing view of the role of oxidative stress in ageing is the trade-off principle which states that a phenotypic trait can be evolutionarily conserved because of its positive effects on development, growth or fertility, and despite its negative effect on somatic functions and ageing. It is likely that most cellular stresses which comprise adaptive and toxic functions follow such a rule.
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PMID: 16527207 [PubMed - indexed for MEDLINE]
72: Clin Biochem. 2006 Mar;39(3):293-8. Epub 2006 Feb 21.
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Cytotoxic effects of volatile anesthetics with free radicals undergoing laparoscopic surgery.
Sivaci R, Kahraman A, Serteser M, Sahin DA, Dilek ON.
Department of Anesthesiology, Afyon Kocatepe University, Afyon 03200, Turkey. rsivaci@aku.edu.tr
BACKGROUND: Free radicals induced by several diseases can trigger oxidative stress, leading to the production of malondialdehyde (MDA) and protein carbonyl content (CB). Volatile agents are able to increase the extent of oxidative status. However, the effects of these agents together with pneumoperitonium (Pp) have not been reported. We aimed to investigate the role of volatile anesthetics and ischemic injury during Pp on free radicals and scavenging enzymes in laparoscopic abdominal surgery. METHODS AND MATERIALS: Forty patients were examined. Patients were randomly divided into four groups in order to receive sevoflurane-fentanyl (SF = 10), sevoflurane-N(2)O (SN = 10), desflurane-fentanyl (DF = 10), and desflurane-N(2)O (DN = 10), respectively. Tidal volume and ventilation frequency were kept unchanged during the operation. Intraabdominal pressure was remained constant at 12 mm Hg. Baseline values in venous blood samples were preoperatively taken and blood was also taken postoperatively at the 6th and the 24th hours. After collection of blood samples into citrate (3.5 mg/mL blood) containing glass tubes, erythrocyte sediments were prepared for the analyses. Then malondialdehyde levels, protein carbonyl content, and sulfhydryl (SH) groups were measured. RESULTS: The levels of MDA and protein carbonyl content were significantly higher at the 6th hour rather than the 24th hour postoperatively with desflurane anesthesia. In addition, SH groups were significantly different between the 6th hour and the 24th hour measurements (P < 0.05). In our study, desflurane caused a statistically significant increase in MDA levels and protein carbonyl content and a decrease in SH groups. When the two groups were compared, in the case of MDA and CB values, a significant increase was observed in the 6th and the 24th hour, where there was a decrease in SH groups in the desflurane group (P < 0.05). These parameters did not change in the sevoflurane group (P > 0.05). CONCLUSION: We concluded that desflurane was affected by desflurane with low flow anesthesia in patients undergoing laparoscopic abdominal surgery. Significant influence on oxidative stress and antioxidant mechanics was not seen with sevoflurane anesthesia. Our studies support that oxidant and antioxidant defense mechanisms were altered in the desflurane group and this alteration improved after a combination of desflurane-N(2)O.
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PMID: 16494857 [PubMed - indexed for MEDLINE]
73: J Neurosci Res. 2006 May 1;83(6):1048-57.
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Huperzine A attenuates mitochondrial dysfunction in beta-amyloid-treated PC12 cells by reducing oxygen free radicals accumulation and improving mitochondrial energy metabolism.
Gao X, Tang XC.
State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, People's Republic of China.
We observed previously that huperzine A (HupA), a selective acetylcholinesterase inhibitor, can counteract neuronal apoptosis and cell damage induced by several neurotoxic substances, and that this neuroprotective action somehow involves the mitochondria. We investigated the ability of HupA to reduce mitochondrial dysfunction in neuron-like rat pheochromocytoma (PC12) cells exposed in culture to the amyloid beta-peptide fragment 25-35 (Abeta(25-35)). After exposure to 1 microM Abeta(25-35) for various periods, cells exhibited a rapid decline of ATP levels and obvious disruption of mitochondrial membrane homeostasis and integrity as determined by characteristic morphologic alterations, reduced membrane potential, and decreased activity of ion transport proteins. In addition, Abeta(25-35) treatment also led to inhibition of key enzyme activities in the electron transport chain and the tricarboxylic acid cycle, as well as an increase of intracellular reactive oxygen species (ROS). Pre-incubation with HupA for 2 hr not only attenuated these signs of cellular stress caused by Abeta, but also enhanced ATP concentration and decreased ROS accumulation in unharmed normal cells. Those results indicate that HupA protects mitochondria against Abeta-induced damages, at least in part by inhibiting oxidative stress and improving energy metabolism, and that these protective effects reduce the apoptosis of neuronal cells exposed to this toxic peptide. 2006 Wiley-Liss, Inc.
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PMID: 16493671 [PubMed - indexed for MEDLINE]
74: Comp Biochem Physiol B Biochem Mol Biol. 2006 Apr;143(4):391-6. Epub 2006 Feb 14.
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Free radicals, lipid peroxidation and the antioxidant system in the blood of cows and newborn calves around calving.
Gaál T, Ribiczeyné-Szabó P, Stadler K, Jakus J, Reiczigel J, Kövér P, Mézes M, Sümeghy L.
Department of Internal Medicine, Faculty of Veterinary Science, Szent István University, István u. 2, Budapest, H-1078, Hungary. Gaal.Tibor@aotk.szie.hu
The oxidative stress of birth in cattle (Bos taurus) was evaluated by measuring steady state concentration of free radicals in whole blood, rate of lipid peroxidation and activity of antioxidant enzymes in erythrocytes, antioxidant capacity of blood plasma in 14 calves at birth and four times after birth until 3 weeks of age and also in their mothers at calving. The same parameters were also measured in 58 dairy cows before calving, at parturition and after calving. Free radical concentration in the blood of newborn calves was higher than in cows confirming that birth means oxidative stress for calves. Red blood cell malondialdehyde in calves was the highest at birth and following the first solid feed intake at the third week. Superoxide dismutase activity increased in calves during the first three weeks of life. Ferric reducing ability of plasma was higher in calves at birth than in cows and decreased thereafter. Higher superoxide dismutase activity in red blood cells and lower ferric reducing ability of plasma in dairy cows was found at calving compared to the average of all pre- and post-calving results. We conclude that the blood of newborn calves is well prepared to deal with the oxidative stress of birth, and that such a stress is present even when some fingerprint markers of redox imbalance show no apparent alterations. Stress of calving has minor effects on the antioxidant system of cows.
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PMID: 16478674 [PubMed - indexed for MEDLINE]
75: Intern Med. 2006;45(1):1-4. Epub 2006 Feb 1.
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Edaravone diminishes free radicals from circulating neutrophils in patients with ischemic brain attack.
Aizawa H, Makita Y, Sumitomo K, Aburakawa Y, Katayama T, Nakatani-Enomoto S, Suzuki Y, Fujiwara K, Enomoto H, Kuroda K, Kimura T, Yahara O, Koyama S, Maruyama J, Nakamura M, Hasebe N, Kikuchi K.
The First Department of Medicine, Asahikawa Medical College, Asahikawa
OBJECTIVE: Treatment with a free radical scavenger could be a new option for ischemic brain attack, however, little is known about the alteration of oxidative stress markers induced by edaravone, a novel free radical scavenger, in human ischemic brain attack. METHODS: We investigated the effects of edaravone on the oxidative stress markers in patients with ischemic brain attack. Twenty-one patients with ischemic brain attack and 19 controls were enrolled in this study. Blood samples were obtained just before and soon after the first administration of edaravone (30 mg) or ozagrel (40 mg). Intracellular reactive oxygen species of neutrophils were measured using 6-carboxy-2', 7'-dichlorodihydrofluorescin diacetate and a fluorescence-activated cell sorter. Superoxide from neutrophils, induced by phorbol myristate acetate (PMA), was determined by luminol-amplified chemiluminescence assay. RESULTS: Treatment with 30 mg of edaravone significantly decreased the intracellular reactive oxygen species (ROS) of neutrophils (Wilcoxon test, p=0.0001) and PMA-induced superoxide produced by neutrophils (Wilcoxon test, p=0.001). Ozagrel did not alter the intracellular ROS or superoxide production of neutrophils. CONCLUSION: Reduction of intracellular ROS and suppression of superoxide production in neutrophils provide a potential explanation for the clinical efficacy of edaravone in patients with ischemic brain attack.
PMID: 16467596 [PubMed - indexed for MEDLINE]
76: Free Radic Biol Med. 2006 Feb 1;40(3):388-97. Epub 2005 Nov 9.
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Free radicals, mitochondria, and hypoxia-ischemia in the developing brain.
Blomgren K, Hagberg H.
Arvid Carlsson Institute, Sahlgrenska Academy, Göteborg University, Sweden. klas.blomgren@neuro.gu.se
The immature brain is particularly susceptible to free radical injury because of its poorly developed scavenging systems and high availability of iron for the catalytic formation of free radicals. Neurons are more vulnerable to free radical damage than glial cells, but oligodendrocyte progenitors and immature oligodendrocytes in very prematurely born infants are selectively vulnerable to depletion of antioxidants and free radical attack. Reactive oxygen and nitrogen species play important roles in the initiation of apoptotic mechanisms and in mitochondrial permeability transition, and therefore constitute important targets for therapeutic intervention. Oxidative stress is an early feature after cerebral ischemia and experimental studies targeting the formation of free radicals demonstrate various degrees of protection after perinatal insults. Oxidative stress-regulated release of proapoptotic factors from mitochondria appears to play a much more important role in the immature brain. This review will summarize and compare with the adult brain some of the current knowledge of free radical formation in the developing brain and its roles in the pathophysiology after cerebral hypoxia-ischemia.
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PMID: 16443153 [PubMed - indexed for MEDLINE]
77: Chem Biol Interact. 2006 Mar 10;160(1):1-40. Epub 2006 Jan 23.
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Free radicals, metals and antioxidants in oxidative stress-induced cancer.
Valko M, Rhodes CJ, Moncol J, Izakovic M, Mazur M.
Faculty of Chemical and Food Technology, Slovak Technical University, SK-812 37 Bratislava, Slovakia. marian.valko@stuba.sk
Oxygen-free radicals, more generally known as reactive oxygen species (ROS) along with reactive nitrogen species (RNS) are well recognised for playing a dual role as both deleterious and beneficial species. The "two-faced" character of ROS is substantiated by growing body of evidence that ROS within cells act as secondary messengers in intracellular signalling cascades, which induce and maintain the oncogenic phenotype of cancer cells, however, ROS can also induce cellular senescence and apoptosis and can therefore function as anti-tumourigenic species. The cumulative production of ROS/RNS through either endogenous or exogenous insults is termed oxidative stress and is common for many types of cancer cell that are linked with altered redox regulation of cellular signalling pathways. Oxidative stress induces a cellular redox imbalance which has been found to be present in various cancer cells compared with normal cells; the redox imbalance thus may be related to oncogenic stimulation. DNA mutation is a critical step in carcinogenesis and elevated levels of oxidative DNA lesions (8-OH-G) have been noted in various tumours, strongly implicating such damage in the etiology of cancer. It appears that the DNA damage is predominantly linked with the initiation process. This review examines the evidence for involvement of the oxidative stress in the carcinogenesis process. Attention is focused on structural, chemical and biochemical aspects of free radicals, the endogenous and exogenous sources of their generation, the metal (iron, copper, chromium, cobalt, vanadium, cadmium, arsenic, nickel)-mediated formation of free radicals (e.g. Fenton chemistry), the DNA damage (both mitochondrial and nuclear), the damage to lipids and proteins by free radicals, the phenomenon of oxidative stress, cancer and the redox environment of a cell, the mechanisms of carcinogenesis and the role of signalling cascades by ROS; in particular, ROS activation of AP-1 (activator protein) and NF-kappaB (nuclear factor kappa B) signal transduction pathways, which in turn lead to the transcription of genes involved in cell growth regulatory pathways. The role of enzymatic (superoxide dismutase (Cu, Zn-SOD, Mn-SOD), catalase, glutathione peroxidase) and non-enzymatic antioxidants (Vitamin C, Vitamin E, carotenoids, thiol antioxidants (glutathione, thioredoxin and lipoic acid), flavonoids, selenium and others) in the process of carcinogenesis as well as the antioxidant interactions with various regulatory factors, including Ref-1, NF-kappaB, AP-1 are also reviewed.
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PMID: 16430879 [PubMed - indexed for MEDLINE]
78: J Orthop Res. 2006 Jan;24(1):55-62.
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Role of free radicals in aseptic loosening of hip arthroplasty.
Kinov P, Leithner A, Radl R, Bodo K, Khoschsorur GA, Schauenstein K, Windhager R.
Department of Orthopaedic Surgery, Medical University of Graz, Auenbruggerplatz 5, A-8036 Graz, Austria.
Fibrous pseudocapsule around hip implants is an invariable finding at revision operations and is believed to release inflammatory mediators that stimulate bone resorption. Reactive oxygen species have been proposed to be causative factors in various disorders with tissue fibrosis. We were interested in investigating whether aseptic loosening is connected with high oxidative stress, and in showing the underlying mechanism of periprosthetic fibrosis and its role in loosening. Levels of oxidative stress markers reduced (GSH) and oxidized (GSSG) gluthatione and malondialdehyde (MDA) were assayed in 28 loose hips and in 12 stable hips revised for high rate of wear and osteolysis. Collagen in the periprosthetic tissues was measured as hydroxyproline content. Osteolysis and polyethylene wear were graded. Increased oxidative stress measured by low GSH/GSSG ratio as well as by increased MDA level was established in patients compared to controls. Oxidative stress markers intercorrelated significantly. MDA and both GSH and GSSG levels correlated significantly with hydroxyproline level. Levels of GSSG and MDA were higher in hips with greater polyethylene wear. The results suggest that high oxidative stress may play a role in formation of a fibrous membrane observed at revision of loose hips. The fibrous pseudocapsule is probably related to high intraarticular pressure and expansion of the effective joint space. This study may elicit some aspects of the pathogenesis of aseptic hip loosening and aid in future investigations aiming at prevention of this complication.
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PMID: 16419969 [PubMed - indexed for MEDLINE]
79: Urology. 2006 Jan;67(1):2-8.
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What an andrologist/urologist should know about free radicals and why.
Agarwal A, Prabakaran S, Allamaneni S.
Center for Advanced Research in Human Reproduction, Infertility, and Sexual Function, Glickman Urological Institute, Cleveland, Ohio 44195, USA. Agarwaa@ccf.org
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PMID: 16413322 [PubMed - indexed for MEDLINE]
80: J Neurosci Res. 2006 Feb 1;83(2):256-63.
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Protein glutathionylation in human central nervous system: potential role in redox regulation of neuronal defense against free radicals.
Sparaco M, Gaeta LM, Tozzi G, Bertini E, Pastore A, Simonati A, Santorelli FM, Piemonte F.
Division of Neurology, Department of Neurosciences, Azienda Ospedaliera G. Rummo, Benevento, Italy.
Neuronal defense against free radicals is mediated primarily by the glutathione system. A cerebral defect of this system gives rise to the oxidative stress occurring in some neurological diseases. Glutathione provides a means of regulating protein function by glutathionylation, consisting of the formation of mixed disulfides between cysteines and glutathione. The glutathionylation of proteins, during both constitutive metabolism and oxidative stress, represents for the cell a mechanism to link physiological processes, and/or adaptive stress responses, to changes in intracellular redox states. In this study, we analyzed the topographic distribution of the protein glutathionylation normally occurring in human central nervous system. Constitutively glutathionylated proteins appeared uniformly distributed throughout all cortical layers of the cerebral and cerebellar cortex as well as throughout the gray matter of the spinal cord. The degree of immunocytochemical staining was clear in neurons, mild in oligodendrocytes, and weaker in astrocytes. The proteins preferentially glutathionylated were cytoskeletal proteins. Our results suggest a potential role of glutathionylation in the redox regulation of neuronal survival and in the control of axon/dendrite stability. Copyright 2005 Wiley-Liss, Inc.
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PMID: 16385584 [PubMed - indexed for MEDLINE]
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