PubMed Health⌕ Search

Biomedical subjects

Müjdat Uysal

Publications and source records attributed to Müjdat Uysal.

At least 19 recordsLinked to original sources

The effect of heme oxygenase-1 induction by glutamine on radiation-induced intestinal damage: the effect of heme oxygenase-1 on radiation enteritis.

BACKGROUND: Radiation enteritis is a significant clinical problem in patients receiving ionizing radiation directed at the abdomen or pelvis. The small intestine is the most radiosensitive gastrointestinal organ. Myeloperoxidase (MPO) activity and malondialdehyde (MDA) levels of the small intestine were measured to determine the oxidative damage caused by radiation. In addition, caspase-3 activity of the small intestine was measured to define the degree of apoptosis. The present study was undertaken to investigate the effect of glutamine administration on heme oxygenase-1 (HO-1) expression of the radiation enteritis model. METHODS: Rats received 1 g/kg/d glutamine (HO-1-inducer) for 7 days before irradiation and continued for 3 days after irradiation. Zn-prothoporphyin (Zn-PP) 40 micromol/kg was delivered subcutaneously for 1 day before irradiation. Intestinal MPO activities and MDA levels are indicators of oxidative damage, whereas caspase-3 activities show the degree of apoptosis of the small intestine. At histopathologic examination, terminal ileum tissue was analyzed for morphologic changes. Also, the nuclear factor-kappa (NF-kappa) expression level of the terminal ileum was determined with immunohistochemistry methods to show the mucosal inflammatory process. RESULTS: Irradiation significantly increased the intestinal MPO and caspase-3 activities, MDA levels, and HO-1 expression in comparison with the sham group. Glutamine treatment was associated with increased HO-1 expression, decreased MPO activity, caspase-3 activity, and MDA levels. Inhibition of HO-1 activity by Zn-PP completely eliminated the protective effects of glutamine. Histopathologic examination showed that the intestinal mucosal structure was preserved in the glutamine-treated group. In the irradiation group, NF-kappaB overexpression was detected. NF-kappaB positivity was strongest in the intestine of animals in the radiation alone group and the Zn-PP-treated irradiation group. CONCLUSIONS: Glutamine appears to have protective effects against radiation-induced intestinal damage. This protective effect is mediated in part by the induction of HO-1 activity because inhibition of Zn-PP resulted in the complete abolishment of the protective effect of glutamine.

Animals↗

The effect of heme oxygenase-1 induction by octreotide on radiation enteritis.

Radiation enteritis occurs as a response to abdominal radiation, which can cause mucosal damage in the gastrointestinal mucosal epithelium. The small intestine is one of the most radiosensitive organs in the abdomen. The present study was undertaken to investigate the effect of octreotide (OCT) administration on heme oxygenase-1 (HO-1) expression of the radiation enteritis model. Rats received 50 mg/kg/day OCT for 4 days before irradiation and continued for 3 days after irradiation. Intestinal myeloperoxidase (MPO) activities, malondialdehyde (MDA) levels are indicators of oxidative damage while caspase-3 activities reveal apoptosis degree of the small intestine. At histological examination, the terminal ileum tissue was analyzed for morphological changes. Irradiation significantly increased the intestinal MPO and caspase-3 activities, MDA levels and HO-1 expression in comparison to sham control group. OCT treatment was associated with increased HO-1 expression and caspase-3 activity, decreased MPO activity and MDA levels. Histological examination revealed that the intestinal mucosal structure was preserved in the OCT treated group. OCT appears to have protective effects against radiation-induced intestinal damage. This protective effect is, in part, mediated by modification of the inflammatory response and the induction of HO-1 expression.

Animals↗

Increased plasma malondialdehyde and protein carbonyl levels and lymphocyte DNA damage in patients with angiographically defined coronary artery disease.

We investigated the oxidative modifications of lipids, proteins and DNA, three potential molecular targets of oxidative stress, in 30 patients with angiographically defined coronary artery disease (CAD) and 30 healthy control subjects. In addition, we examined relationships between these oxidative modifications and the severity of vascular lesions in patients with CAD. Malondialdehyde (MDA) and protein carbonyl (PC) levels, as well as ferric reducing antioxidant power (FRAP), were measured in the plasma. DNA damage was evaluated as single strand breaks (SSBs), formamidopyrimidine glycosylase (Fpg) and endonuclease III (E-III)-sensitive sites by the comet assay in DNA isolated from lymphocytes. MDA and PC levels increased, but FRAP values decreased, in patients as compared to controls. However, these values did not vary with the number of affected coronary vessels and were not correlated with Duke score, a parameter of the severity of vascular lesions in patients with CAD. We also found that lymphocyte DNA damage (SSBs, Fpg and E-III sites) were increased in patients. Although there were no significant differences in SSBs values in patients grouped according to affected vessel number, Fpg and E-III sites increased. We also detected significant correlations between Duke scores and SSBs and Fpg sites. Serum cholesterol, triglyceride and LDL-cholesterol levels were found to increase, but HDL-cholesterol levels decreased in CAD patients, but these lipids were not correlated with Duke scores. The results of this study reinforce the presence of increased combined oxidative modifications in lipid, protein and DNA in patients with CAD. However, lymphocyte DNA damage seems to be a more reliable assay than MDA and PC determinations to detect the severity of vascular lesions in patients.

Adult↗

Peroxynitrite induced decrease in Na+, K+-ATPase activity is restored by taurine.

AIM: Peroxynitrite (ONOO-) is a powerful oxidant shown to damage membranes. In the present study, the effect of taurine on changes of liver plasma membrane Na+, K+-ATPase induced by ONOO- was investigated. METHODS: Liver plasma membrane was exposed to ONOO- with or without taurine. Na+, K+-ATPase activity and lipid peroxidation as thiobarbituric acid reactive substances (TBARS) levels were measured. RESULTS: Different concentrations of ONOO- (100, 200, 500, and 1000 micromol/L) were found to decrease liver plasma membrane Na+, K+-ATPase activity significantly. The depletion of enzyme activity was not concentration dependent. Effects of different concentrations of taurine on liver plasma membrane Na+, K+-ATPase activity were also measured. Taurine did not cause any increase in enzyme activity. When plasma membranes were treated with 200 micromol/L ONOO- with different concentrations of taurine, a restoring effect of taurine on enzyme activity was observed. TBARS levels were also measured and taurine was found to decrease the elevated values. CONCLUSION: Taurine is observed to act as an antioxidant of ONOO- to decrease lipid peroxidation and thus affect liver plasma membrane Na+, K+-ATPase by restoring its activity.

Animals↗

Induced oxidative stress and decreased expression of inducible heat shock protein 70 (ihsp 70) in patients with colorectal adenocarcinomas.

BACKGROUND: Colorectal cancer is one of the most common carcinomas observed in humans. Recently we have reported that increased oxidative stress is associated with human colorectal cancer. There are few and controversial studies on the clinical relevance of the expression of heat shock protein 70 (HSP 70), a member of the HSP family, in colorectal cancer. In this study, we assayed lipid peroxide levels, glutathione peroxidase (GPx) activity and the expression of inducible heat shock protein 70 (ihsp 70) in 20 paired samples of colorectal tumor and adjacent normal tissues in order to determine the relationship between oxidative stress and ihsp 70 expression. Histopathological results were also considered to establish the clinical relevance of ihsp 70 in colorectal cancer. METHODS: Malondialdehyde (MDA) levels as an indicator of lipid peroxidation and GPx activity were assayed by spectrophotometric methods. The Western blotting procedure was used for the determination of ihsp 70 expression. RESULTS: Significant increases were observed in MDA levels (111%) and GPx activities (50%) of malignant tissues as compared with normal tissues of the patients with colorectal cancer. The expression of ihsp 70 was found to be decreased in malignant tissues as compared with normal tissues of the patients. Significant negative correlations were detected between MDA levels and ihsp expression (r = -0.516; P < 0.05 ) and GPx activity and ihsp 70 expression (r = -0.471; P < 0.05) in malignant tissues of patients. When the patients were grouped according to histopathological characteristics, no difference was found in MDA levels, GPx activity and ihsp 70 expression. CONCLUSION: Our results indicate that ihsp70 expression is suppressed under induced oxidative stress conditions in malignant tissues of patients with colorectal cancer. Further research is needed to clarify the mechanisms responsible for this decrease and the definitive role of ihsp 70 in colorectal cancer.

Adenocarcinoma↗

The effect of taurine or betaine pretreatment on hepatotoxicity and prooxidant status induced by lipopolysaccharide treatment in the liver of rats.

BACKGROUND: Taurine or betaine have been reported to have antioxidative potential and inhibit Kupffer cell activation. These effects may play an important role in their hepatoprotective effects. Therefore, they may also have protective effects in lipopolysaccharide hepatotoxicity by both inhibiting Kupffer cell activation and behaving as antioxidants. DESIGN: The prophylactic efficiency of taurine or betaine pretreatment for the prevention of peroxidative changes induced by lipopolysaccharide treatment in the rat liver was investigated. METHODS: Lipopolysaccharide (10 mg/kg intraperitoneally) was given to rats pretreated with taurine (1.5%, w/v) or betaine (1.5%, w/v) in drinking water for 4 weeks and plasma transaminase activities as well as hepatic malondialdehyde, diene conjugate (DC), glutathione, alpha-tocopherol and ascorbic acid levels, and superoxide dismutase (SOD) and glutathione peroxidase activities were determined. RESULTS: Significant increases in plasma transaminase activities and hepatic malondialdehyde and DC levels and decreases in hepatic glutathione and alpha-tocopherol levels and SOD and glutathione peroxidase activities were observed 6 h after lipopolysaccharide treatment. This treatment did not alter ascorbic acid levels in the liver compared with controls. Taurine or betaine pretreatment in lipopolysaccharide-injected rats caused significant decreases in plasma transaminase activities and hepatic malondialdehyde and DC levels, and significant increases in glutathione and alpha-tocopherol (not betaine) levels without changing ascorbic acid levels and SOD and glutathione peroxidase activities in the liver. CONCLUSIONS: Our findings clearly indicate that taurine or betaine pretreatment was effective in the prevention of lipopolysaccharide-induced hepatotoxicity and prooxidant status.

Animals↗

Increased LDL+VLDL oxidizability and plasma homocysteine levels in chronic alcoholic patients.

The purpose of this study was to investigate the effect of heavy alcohol consumption on peroxidation status in apolipoprotein B-containing lipoproteins (LDL+VLDL) and plasma as well as plasma homocysteine (HC) levels in patients with chronic alcoholism who drank raki, a national Turkish beverage. For this reason, endogenous diene conjugate (DC) and lipid hydroperoxide (LOOH) levels and lag phase, maximum DC formation and propagation rate following copper induction were measured in apolipoprotein B-containing lipoproteins (LDL+VLDL) isolated by precipitation with dextrane sulfate and MgCl2 from plasma. In addition, serum malondialdehyde (MDA), DC, HC, folate and vitamin B12 levels as well as paraoxonase activity were determined. Serum MDA and DC levels were higher in heavy raki drinkers compared to control subjects. Significant increases in endogenous DC and LOOH levels in LDL+VLDL together with shortened lag phase were also observed in patients. In addition, HDL-cholesterol, HC and vitamin B12 levels and HDL-associated paraoxonase activity were found to be higher, but folate levels to be lower in serum of heavy raki consumers. In conclusion, our results indicate that increases in LDL+VLDL oxidizability and plasma HC levels may enhance the susceptibility to vascular diseases in heavy raki drinkers.

Adult↗

Heme oxygenase induction protects liver against oxidative stress in x-irradiated aged rats.

We studied the effect of total body X-ray irradiation on the heme oxygenase-1 (HO-1) induction in the livers of young and aged rats. For this purpose, male rats were irradiated with a dose of 17 Gy. The animals were killed 5 h after irradiation. HO-1 protein expression was found to be increased two fold in aged rat liver, but lipid peroxide levels had decreased significantly where no change was observed either in inducible nitric oxide synthase protein expression or in glutathione levels. Contradictory results with respect to HO-1 and lipid peroxidation levels were obtained in the livers of young animals. These results suggest that the additional oxidative stress produced in irradiated rats may be compensated by HO-1 induction as decreased lipid peroxide levels were shown in the livers of aged animals.

Aging↗

Melatonin improved the disturbances in hepatic prooxidant and antioxidant balance and hepatotoxicity induced by a high cholesterol diet in C57BL/6J mice.

We examined the effect of melatonin in prooxidant and antioxidant state in the liver of C57BL/6J mice fed on a high cholesterol (HC) diet. Mice were fed with normal mice chow containing 1.5% cholesterol and 0.5% cholic acid for 4 months without and with melatonin (10 mg/L in drinking water) treatment. HC diet was observed to increase malondialdehyde (MDA) and diene conjugate (DC) levels in the liver. This diet lowered glutathione (GSH), alpha-tocopherol, and total ascorbic acid levels as well as glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities in the liver, but hepatic superoxide dismutase (SOD) activity remained unchanged. Although melatonin treatment did not affect these parameters in mice fed a normal diet, it reduced hepatic MDA and DC levels in mice fed an HC diet. Hepatic alpha-tocopherol and ascorbic acid levels increased, but hepatic GSH levels remained unchanged in the melatonin-treated HC group as compared to the HC group. Melatonin treatment was found to increase liver GSH-Px and GST activities in mice fed an HC diet. However, SOD activity did not alter in the liver of hypercholesterolemic mice following melatonin treatment. In addition, the histopathological lesions observed in the cholesterol-plus-melatonin group were less severe than those seen in the cholesterol group. According to these observations, we can say that melatonin treatment has an ameliorating effect on the disturbances in prooxidant and antioxidant balance and histopathological lesions in the liver of mice following cholesterol feeding.

Animals↗

The effect of betaine treatment on triglyceride levels and oxidative stress in the liver of ethanol-treated guinea pigs.

We investigated the effect of betaine supplementation on ethanol induced steatosis and alterations in prooxidant and antioxidant status in the liver of guinea pigs. Animals were fed with normal chow or betaine containing chow (2% w/w) for 30 days. Ethanol (3 g/kg, i.p.) was given for the last 10 days. We found that ethanol treatment caused significant increases in plasma transaminase activities, hepatic triglyceride and lipid peroxide levels. Significant decreases in glutathione (GSH), alpha-tocopherol and total ascorbic acid (AA) levels were also observed, but hepatic superoxide dismutase, glutathione peroxidase and glutathione transferase activities remained unchanged as compared with those in controls. Betaine treatment together with ethanol in guinea pigs is found to decrease hepatic triglyceride, lipid peroxide levels and serum transaminase activities and to increase GSH levels. No changes in alpha-tocopherol and total AA levels and antioxidant enzyme activities were observed with betaine treatment in alcohol treated guinea pigs. In addition, histopathological assessment of guinea pigs showed that betaine reduced the alcoholic fat accumulation in the liver. Based on these data, betaine treatment has a restoring effect on the alterations in triglyceride, lipid peroxide and GSH levels following ethanol ingestion.

Alanine Transaminase↗

Melatonin reduces cholesterol accumulation and prooxidant state induced by high cholesterol diet in the plasma, the liver and probably in the aorta of C57BL/6J mice.

We examined the hypolipidemic and antioxidative effects of melatonin in plasma, liver and aorta of C57BL/6J mice fed on a high cholesterol (HC) diet. Mice were fed normal mice chow containing 1.5% cholesterol and 0.5% cholic acid for 4 months with or without melatonin (10 mg/L in drinking water) treatment. HC diet was observed to increase cholesterol, triglyceride and diene conjugate (DC) levels in plasma and liver. There was a tendency towards an increase in cholesterol level in the aorta following HC diet. In addition, aortic DC levels were higher than those of control group. No fatty streaks or plaques developed in the aorta of mice following HC diet, but in some sections, derangement of the endothelial layer was detected. Melatonin treatment was found to reduce plasma, liver cholesterol and DC levels as well as liver triglyceride levels in hypercholesterolemic mice. Aortic cholesterol and DC levels were also reduced in hypercholesterolemic mice when given melatonin, although not statistically significant. There were no differences in aortic histopathological findings of mice fed on a HC diet with and without melatonin treatment. In conclusion, our results indicate that melatonin reduces HC diet-induced cholesterol accumulation and prooxidant state in the plasma, liver and probably in the aorta.

Animals↗

Effect of a taurine treatment on the regression of existing atherosclerotic lesions in rabbits fed on a high-cholesterol diet.

We studied whether taurine has any regressive effect on existing atherosclerotic lesions and lipid peroxidation in rabbits fed on a high-cholesterol (HC) diet. The cholesterol, triglyceride, malondialdehyde (MDA) and diene conjugate (DC) levels, as well as the aortic histopathological findings were examined in rabbits that had been fed on a cholesterol-containing diet for 8 months [0.5% cholesterol (w/w) for 3 months and subsequently 0.25% cholesterol (w/w) for 5 months], and then for a further 4 months on a normal diet with or without taurine treatment [1% (w/v) in the drinking water]. High levels of lipid and lipid peroxide induced by the HC diet were observed to decline in the plasma, liver and aorta of atherosclerotic rabbits, as well as a slight retardation in aortic atherosclerotic lesions during the regression period. Although no significant differences in the lipid and lipid peroxide levels in the plasma and aorta were found between the regressed groups with or without the taurine treatment, the extent of atherosclerotic lesions in the aorta was less in the taurine-treated regressed group than in the non-treated regressed group. However, the liver MDA and DC levels were lower in the regressed rabbits with the taurine treatment in the non-treated group. These results indicate that the taurine treatment may accelerate the regression of cholesterol-induced atherosclerotic lesions in rabbits without having any effect on the plasma and aorta lipid and lipid peroxide levels.

Animals↗

Hazelnut oil administration reduces aortic cholesterol accumulation and lipid peroxides in the plasma, liver, and aorta of rabbits fed a high-cholesterol diet.

Hazelnut oil (HO) is rich in monounsaturated fatty acids and antioxidants. We wanted to investigate the effect of HO on lipid levels and prooxidant-antioxidant status in rabbits fed a high-cholesterol (HC) diet. An HC diet caused significant increases in lipids and lipid peroxide levels in the plasma, liver, and aorta together with histopathological atherosclerotic changes in the aorta. Glutathione levels, glutathione peroxidase, and glutathione transferase activities decreased significantly, but superoxide dismutase activity and vitamin E and C levels remained unchanged in the livers of rabbits following HC diet. HO supplementation reduced plasma, liver, and aorta lipid peroxide levels and aorta cholesterol levels together with amelioration in atherosclerotic lesions in the aortas of rabbits fed an HC diet, without any decreasing effect on cholesterol levels in the plasma or liver. HO did not alter the antioxidant system in the liver in the HC group. Our findings indicate that HO reduced oxidative stress and cholesterol accumulation in the aortas of rabbits fed an HC diet.

Animals↗

Methionine supplementation did not augment oxidative stress, atherosclerotic changes and hepatotoxicity induced by high cholesterol diet in C57BL/6J mice.

The purpose of this study was to investigate the effect of a high-methionine plus cholesterol diet (HM+HC) on plasma, erythrocyte, liver and aorta lipid, lipid peroxide levels, and the liver antioxidant system, as well as hepatic and aortic histopathology in CS 7BL/6J mice, and to compare these results to those observed following administration of a high-methionine (HM) or high-cholesterol diet (HC) alone. Mice were fed diets containing 1.5% methionine, 1.5%, cholesterol and 0.5% cholic acid, or a combination of the two diets, for 4 mo. The HM diet did not alter cholesterol or diene conjugate (DC) levels in the plasma or aorta, but this diet caused increases in cholesterol, triglyceride, malondialdehyde (MDA) and DC levels and a decrease in a-tocopherol levels without any change in the levels of glutathione and ascorbic acid or the activities of superoxide dismutase, glutathione peroxidase and glutathione transferase in the liver of mice. However, the HC diet alone was found to further increase cholesterol, triglyceride. MDA and DC levels in the plasma and liver together with changes in hepatic antioxidant system elements, but aortic cholesterol and DC levels remained unchanged as compared to the control group. There were no changes in blood hemoglobin and erythrocyte MDA levels or erythrocyte hemolysis values in both the HM and HC groups. However, the parameters related to lipid and lipid peroxide and antioxidant systems did not change in the plasma or tissues of the HM+HC and HC groups. Only plasma cholesterol was observed to increase in the HM+HC group as compared to the HC group. In addition, histopathological findings in the liver and aorta were similar in the HC and HM+HC groups. In conclusion, our results indicate that the addition of methionine to the HC diet did not augment oxidative stress, hepatotoxicity or atherosclerotic changes induced by the HC diet in mice.

Animals↗

Influence on hazelnut oil administration on peroxidation status of erythrocytes and apolipoprotein B 100-containing lipoproteins in rabbits fed on a high cholesterol diet.

Hazelnut oil (HO) is rich in monounsaturated fatty acids (MUFA). The effect of a high cholesterol (HC) diet with and without HO on lipids and lipid peroxide levels in plasma, apolipoprotein B 100-containing lipoproteins (VLDL + LDL), and erythrocytes as well as hematological data was investigated in rabbits. A HC diet caused significant increases in lipid peroxide levels in plasma and apo B-containing lipoproteins together with histopathological atherosclerotic findings in aorta. In addition, this diet resulted in hemolytic anemia associated with increased endogenous diene conjugate (DC) levels, but H(2)O(2)-induced malondialdehyde (MDA) levels remained unchanged in erythrocytes. HO supplementation reduced lipid peroxide levels in plasma and apolipoprotein B 100-containing lipoproteins as well as aortic atherosclerotic lesions in rabbits fed an HC diet without any decreasing effect on lipid levels. In addition, HO was found to reduce hemolytic anemia together with significant decreases in DC and H(2)O(2)-induced MDA levels.

Anemia, Hemolytic↗

Age-related increases in plasma malondialdehyde and protein carbonyl levels and lymphocyte DNA damage in elderly subjects.

OBJECTIVES: Increased oxidative stress has been hypothesized to play an important role in the aging process. A role for oxidative damage in normal aging is supported by studies in experimental animals, but there is limited evidence in humans. To investigate the relationship between the oxidative stress and aging in humans, we determined lipid and protein oxidation in plasma as well as DNA damage in lymphocytes in young and elderly subjects. DESIGN AND METHODS: 55 healthy subjects were divided into young (21-40 years) and elderly (61-85 years) groups. Plasma malondialdehyde (MDA), protein carbonyl (PC) levels, and grade of DNA damage in lymphocytes using comet assay as well as total ferric reducing antioxidant power (FRAP) in plasma were determined in young and elderly subjects. RESULTS: Plasma MDA and PC levels were found to be increased in plasma of elderly subjects as compared to young subjects. Increases in endogenous and H2O2-induced DNA damage were also observed in lymphocytes of elderly subjects. In addition, we detected a significant decrease in FRAP values in elderly subjects. Plasma MDA, PC levels and endogenous and H2O2-induced DNA damage were positively correlated with aging, but negatively with FRAP values. CONCLUSION: We evaluated MDA, PC levels and lymphocyte DNA damage altogether in both young and elderly subjects for the first time. The results of this study strongly support the presence of increased oxidative stress in elderly subjects.

Adult↗

Cholesterol plus methionine feeding do not induce lipid peroxidation and atherosclerotic changes in the rat aorta.

The purpose of this study was to investigate whether cholesterol plus methionine feeding may be a convenient model to produce atherosclerosis in rats, and also to examine the contribution of oxidative stress to this development. For this reason, lipid peroxide levels and antioxidant enzyme activities in the liver and aorta as well as histopathological findings were determined in male Wistar-albino rats fed a diet supplemented with cholesterol plus cholic acid and methionine for six months. This diet was found to increase lipid peroxide levels in the liver of rats. Hepatic glutathione peroxidase (GSH-Px) and catalase (CAT) activities increased, but superoxide dismutase (SOD) activity remained unchanged. In conclusion, cholesterol and methionine feeding in rats did not cause oxidative stress and atherosclerotic changes in the aorta, although hepatic prooxidant-antioxidant balance was affected by this diet.

Animals↗

Increased lipid peroxidation in serum and low-density lipoproteins associated with aging in humans.

This study was carried out in 140 healthy subjects who were divided into three subgroups of age: young (21-40 years), mature (41-60 years), and elderly (61-85 years) to investigate lipid peroxides and the antioxidant system in serum and low-density lipoproteins (LDL). Serum levels of cholesterol and LDL-cholesterol increased with age. The elderly group was found to have higher polyunsaturated fatty acid (PUFA) levels, thiobarbituric acid reactive substances (TBARS), diene conjugates, and lower cholesterol-adjusted vitamin E levels and antioxidant activity (AOA) as compared to the young group. No age-related difference was detected in serum vitamin C levels. Age correlated positively with serum cholesterol, LDL-cholesterol, PUFA, TBARS, diene conjugates, and negatively with cholesterol-adjusted vitamin E levels and AOA. In addition, endogenous LDL diene conjugate levels and the susceptibility of LDL to copper-induced lipid peroxidation increased in elderly subjects as compared with young subjects. In addition, positive correlations were detected between age and LDL endogenous diene conjugate levels and TBARS formation after copper incubation. However, the susceptibility of whole serum to copper-induced lipid peroxidation did not change in young and elderly subjects. Our results show that endogenous lipid peroxide levels in serum and LDL, and the susceptibility of LDL to copper-induced oxidation, increased with aging in humans.

Adult↗