Oxidative stress and potential interventions to reduce oxidative stress in overweight and obesity

PURPOSE: Obesity may be a state of chronic oxidative stress. Oxidative stress may be the mechanism underlying the development of co-morbidities in obesity. This review provides a summary of the available evidence regarding systemic oxidative stress in young, older and clinical obese populations. METHODS: Medline was searched for all available articles published between 1975 and 2006 that evaluated oxidative stress biomarkers in resting conditions or following various interventions in overweight and obese humans. RESULTS: Obesity elevates oxidative stress in young, old and clinical populations as shown by elevations in lipid peroxidation (malondialdehyde, hydroperoxides, 4-hydroxynonenal, isoprostanes, conjugated dienes) or protein oxidation (8-hydroxy-deoxyguanosine). Lipid peroxidation is associated with several indices of adiposity and a low systemic antioxidant defence (i.e. antioxidant enzymes, tissue dietary antioxidants, glutathione). Oxidative stress may be exacerbated with acute exercise, advancing age or co-existing clinical conditions and may be corrected by improving antioxidant defences through fat volume reduction via surgery, pharmacological agents, exercise and/or dietary modification. CONCLUSION: Oxidative stress is related to chronic disease in obesity, but is reversible with one or more interventions described above.     

Modulation of age-related biochemical changes and oxidative stress by vitamin C and glutathione supplementation in old rats

The present study sought to determine whether supplementation of dietary antioxidant ascorbic acid with glutathione (GSH) could ameliorate the age-related increased oxidative stress and changes in hormonal, lipid and copper (Cu) as well as zinc (Zn) levels in 18-month-old rats. The present study demonstrated that supplementation of vitamin C (30 mg) + GSH 100 mg/kg b.w. significantly reduced the concentration of thiobarbituric acid-reactive substances in liver and testes in old male rats as compared with nonsupplemented ones, indicating lower oxidative stress. In addition, testicular GSH was increased but not hepatic GSH. Also, cholesterol and triglycerides were decreased in the serum of supplemented rats. Furthermore, she serum testosterone level was increased in the same supplemented rats. However, the present results show that the thyroid hormones, T3 and T4, were not influenced. Lastly, the concentration of Cu in serum, liver, brain and testes was increased in supplemented old rats. Zn concentration was also increased in the same organs but not in the liver. According to the present study, the supplementation of antioxidants could play an important role in the modulation of the oxidative damage and changes associated with age.     

左旋甲状腺素和维生素E干预对甲状腺功能减退大鼠心肌氧化应激和细胞凋亡的影响

目的 通过研究左旋甲状腺素(LT4)、维生素E(VitE)及二者联合治疗对甲状腺功能减退(甲减)大鼠氧化应激及心肌细胞凋亡的影响,进一步探讨甲减心肌损伤的发生机制及其治疗方法.方法 将SD雄性大鼠分为正常对照组、丙基硫氧嘧啶组(PTU)、LT4治疗组(PTU +LT4)、VitE治疗组(PTU+VitE)、LT4和VitE联合治疗组(PTU+LT4 +VitE).测定血清T3、T4、TSH水平以及血清、心肌组织超氧化物歧化酶(SOD)活性和丙二醛含量;用TUNEL法检测心肌细胞凋亡指数.结果 (1)与正常对照组比较,PTU组、PTU+VitE组T3、T4水平明显降低,TSH显著升高(P＜0.05);与PTU组比较,PTU+LT4组、PTU+LT4 +VitE组T3、T4水平明显升高,TSH显著降低(P＜0.05);PTU组与PTU+VitE组T3、T4、TSH水平差异无统计学意义(P＞0.05).(2)与正常对照组比较,PTU组血清及心肌组织丙二醛含量显著升高(P＜0.05),其他各组之间差异无统计学意义(P＞0.05);与正常对照组比较,PTU组血清SOD活性显著降低(P＜0.05),但心肌组织SOD活性各组之间差异无统计学意义(P＞0.05).(3)与正常对照组比较,PTU组、PTU+VitE组心肌细胞凋亡显著升高(P＜0.05);与PTU组比较PTU+LT4组、PTU+ LT4+ VitE组凋亡显著降低(P＜0.05).结论 LT4、VitE及二者联合治疗可降低甲减大鼠心肌细胞凋亡,其机制可能与甲状腺功能改善和氧化应激水平降低有关.     

牛膝多肽通过抑制氧化应激减轻大鼠心肌缺血/再灌注损伤

目的 探讨牛膝多肽（ABPP）预处理对心肌缺血/再灌注（MI/R）损伤的影响及其机制。方法 建立大鼠MI/R模型,将成年SD大鼠随机分为 Sham（假手术）组、MI/R组、药物预处理（ABPP＋MI/R）组。检测血流动力学、用氯化三苯基四氮唑和伊文思蓝双染法检测心肌梗死(MI)面积、以血浆肌酸激酶（CK）和乳酸脱氢酶（LDH）活性检测心肌损伤情况、以超氧化物、丙二醛（MAD）和超氧化物歧化酶（SOD）含量检测心肌氧化应激以及Western blot方法测定心肌组织中gp91phox的表达。用TUNEL法检测心肌细胞的凋亡指数(AI),荧光分析法检测caspase 3活性。结果 与MI/R组比较,ABPP预处理使左心室上升、下降最大速率（±LVdP/dtmax）升高（P<0.05）,MI面积显著减少〔MI/R组为（36.0±3.0）%,ABPP组为（26.5±3.5）%,P<0.05〕,血浆CK和LDH水平分别降低到（1251±72）U/L和（1961±122）U/L（P<0.05）,TUNEL阳性染色显著降低（P<0.05）,caspase-3的活性增加（P<0.05）,超氧化物蓄积减少（P<0.05）,显着降低了gp91phox的表达（P<0.05）,MDA的含量显著减少（P<0.05）,SOD活性增加（P<0.05）。结论 ABPP降低氧化应激和对MI/R损伤的心肌具有保护作用。     

Hypercholesterolemia-induced oxidative stress in heart and its prevention by vitamin E

Oxygen-free radicals have been implicated in hypercholesteolemic atherosclerosis. It is possible that hypercholesterolemia produces oxidative stress in myocardium. We therefore investigated the effects of a high cholesterol diet in the absence or presence of vitamin E on serum cholesterol and lipid peroxidation product malondialdehyde (MDA), chemiluminescence (M-CL), a measure of antioxidant reserve, and activity of antioxidant enzymes [superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-P_x)] in cardiac muscles of rabbits. Rabbits were divided into four groups: Group I, regular rabbit chow diet; Group II, same as Group I + vitamin E; Group III, high cholesterol diet; Group IV, high cholesterol + vitamin E. The heart was removed under anesthesia at the end of 4 months on their respective diets for various biochemical measurements. Serum cholesterol in Groups III and IV increased to a similar extent. There was an increase in the levels of MDA, M-CL, GSH-P_x activity and a decrease in SOD activity in hypercholesterolemic rabbits in the absence of vitamin E. Vitamin E prevented the hypercholesterolemia-induced changes in cardiac MDA, M-CL, and GSH-P_x. These results suggest that hypercholesterolemia produces oxidative stress in the myocardium which may be due to a decrease in the antioxidant reserve, and that vitamin E is effective in preventing hypercholesterolemia-induced oxidative stress on the myocardium.     

Cordycepin (3′-deoxyadenosine) attenuates age-related oxidative stress and ameliorates antioxidant capacity in rats

Free radical-induced oxidative damage is considered to be the most important consequence of the aging process. The activities and capacities of antioxidant systems of cells decline with increased age, leading to the gradual loss of pro-oxidant/antioxidant balance and resulting in increased oxidative stress. Our investigation was focused on the effects of cordycepin (3′-deoxyadenosine) on lipid peroxidation and antioxidation in aged rats. Age-associated decline in the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST), reduced glutathione (GSH), vitamin C and vitamin E, and elevated levels of malondialdehyde (MDA) were observed in the liver, kidneys, heart and lungs of aged rats, when compared to young rats. Furthermore, serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea, and creatinine were found to be significantly elevated in aged rats compared to young rats. Aged rats receiving cordycepin treatment show increased activity of SOD, CAT, GPx, GR and GST, and elevated levels of GSH, and vitamins C and E such that the values of most of these parameters did not differ significantly from those found in young rats. In addition, the levels of MDA, AST, ALT, urea and creatinine became reduced upon administration of cordycepin to aged rats. These results suggest that cordycepin is effective for restoring antioxidant status and decreasing lipid peroxidation in aged rats.     

Levels of oxidative stress in brain and serum of rats with chronic fluorosis and antagonistic effects of vitamin E

<正>Objective To detect the levels of oxidative stress in brain and serum of rats with chronic fluorosis and the antagonistic effects of vitamin E(Vit E),and to reveal the role of oxidative stress in brain injury.Methods Thirty healthy SD rats were divided into three groups based on body weight by means of a random number table(10 rats     

Melatonin versus vitamin E as protective treatment against oxidative stress after extra-hepatic bile duct ligation in rats

The aims of the present study were first to compare the effects of melatonin and vitamin E on the cholestasis syndrome and their protective effect on liver injury, and second, to evaluate the activity of antioxidant enzymes after treatment with these antioxidant drugs. Cholestasis was achieved in adult male Wistar rats by double ligature and section of the extra-hepatic biliary duct. Hepatic and plasma oxidative stress markers were evaluated by changes in the amount of lipid peroxides, measured as malondialdehyde (MDA) and reduced glutathione (GSH) in plasma and homogenates of hepatic tissue. Serum bilirubin, alkaline phosphatase (AP), and gamma-glutamyl-transpeptidase (GGT) were used to evaluate the severity of cholestasis, and serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were used to evaluate the hepatic injury. Both vitamin E and melatonin were administrated 1 day before and 7 days after bile duct ligation. Acute ligation of the bile duct was accompanied by a significant increased in MDA and a decrease in GSH levels in both plasma and liver, as well as a significant reduction in antioxidant enzymes activities. The overall analysis of both treatments showed that melatonin (500 microg/kg daily) offered significantly better protection against cholestasis and a superior protective effect on hepatic injury than did vitamin E (15 mg/kg daily). Although vitamin E treatment resulted in a reduction of parameters of oxidative stress, the results were significantly better after a much lower daily dose of melatonin. Moreover, melatonin treatment was associated with a significant recovery of antioxidative enzymes. In conclusion, the present paper demonstrates a correlation between the intensity of biliary tract obstruction and increased free radical generation, as well as a direct correlation between the level of oxidative stress and the biochemical markers of liver injury. Melatonin (at a much lower dose than vitamin E) was much more efficient than vitamin E in reducing the negative parameters of cholestasis, the degree of oxidative stress and provided a significantly greater hepatoprotective effect against the liver injury secondary to the acute ligation of the biliary duct.     

Simvastatin and losartan enhance nitric oxide and reduce oxidative stress in salt-induced hypertension

BACKGROUND: The renin-angiotensin-aldosterone system and oxidative stress play a major role in the pathogenesis of hypertension. METHODS: We examined the effects of simvastatin, an HMG-CoA inhibitor, and losartan, an angiotensin type 1 receptor antagonist, in Dahl rats fed a high salt diet (8% NaCl), and treated with either simvastatin (3 mg/kg/d), losartan (10 mg/kg/d), or their combination using the drinking water as vehicle, for 3 weeks. Mean blood pressure (MAP) was measured by tail-cuff plethysmography. Plasma levels of nitric oxide (NO) and prostanoids, as well as plasma and tissue angiotensin II (Ang II) and aldosterone (ALDO) were analyzed by enzyme immunoassay. Renal and aortic superoxide production was determined by fluorescence spectrometry. Vascular reactivity of second-order mesenteric arteries was assessed in vitro. RESULTS: Simvastatin, losartan, and the drug combination attenuated the salt-induced increase in MAP. Plasma NO was elevated by simvastatin, losartan, and the combination, whereas plasma thromboxane was reduced by losartan. Simvastatin, losartan, and the combination reduced renal Ang II, but only the combination reduced cardiac Ang II. Heart and renal ALDO were reduced by simvastatin, losartan, and the combination. Aortic and renal NADPH-dependent superoxide production was reduced by simvastatin, losartan, and the combination. The response to acetylcholine, in mesenteric arteries preconstricted with norepinephrine, was greater in the losartan group. CONCLUSIONS: Thus, treatment with simvastatin and losartan lowered oxidative stress and improved endothelial function. Simvastatin significantly reduced the effect of losartan on vascular reactivity in mesenteric arteries, suggesting that their combination may be contraindicated.     

Allium vegetable diet can reduce the exercise-induced oxidative stress but does not alter plasma cholesterol profile in rats

AIMS AND METHODS: This study investigated the effect of Allium vegetable intake on the antioxidative activity and on the plasma cholesterol profile during exercise in rats. Ninety rats were fed either a control diet or a diet with added Allium sativum (AS), Allium cepa (AC), Allium fistulosum (AF), or Allium tuberosum (AT) for 4 weeks and were then subdivided into three groups: before exercise (BE), during exercise (DE), and after exercise (AE). The DE group was exercised on a treadmill for 1 h immediately before being sacrificed. Animals in the AE group were allowed to take a rest for 2 h after having been exercised like the DE group. The antioxidative activity of the Allium vegetables was evaluated with the activities of catalase in plasma and superoxide dismutase (SOD), the ratio of reduced glutathione/oxidized glutathione (GSH/GSSG) and the level of malondialdehyde (MDA) in liver. The plasma concentrations of triglyceride, total cholesterol, and high-density lipoprotein cholesterol were also compared. RESULTS: In AS, AC, AF and AT animals, the ratios of GSH/GSSG were significantly higher than those of the control animals in BE and AE. The level of liver MDA was lower than that of control animals in AE. Compared to control animals, catalase activity of AS animals was higher in BE but was lower in AE while SOD activity of AS animals was lower in both BE and AE. Catalase activity of AC animals was higher in BE and DE while SOD activity of AC animals was higher in DE. There were no differences between AF and control in catalase activities regardless of exercise. There were no differences between control animals and AT animals in SOD activities regardless of exercise. Plasma cholesterol profiles were not significantly different in rats fed different Allium vegetable diets. CONCLUSION: It is suggested that Allium vegetable diets have antioxidative activities and can reduce the oxidative stress that results from exercise in rats but do not alter the plasma cholesterol profile.     

Cardiac oxidative stress in acute and chronic isoproterenol-infused rats

OBJECTIVE: Sympathetic nervous system activity in the myocardium is increased in patients with heart failure. However, the in vivo mechanisms responsible for beta-adrenoceptor-mediated cardiac hypertrophy or remodeling remain unclear. This study aimed to clarify the role of reactive oxygen species (ROS) in mitogen-activated protein (MAP) kinase activation and tissue remodeling of the heart of isoproterenol (ISO)-infused rats. METHODS AND RESULTS: Different doses of ISO (up to 1000 ng/kg/min) were given intravenously to conscious rats for 30 min. Phosphorylated MAP kinase levels (ERK1/2, JNK, p38) and lipid peroxidation were measured in the cardiac left ventricle, revealing the dose-dependent augmentation of MAP kinase phosphorylation and increased lipid peroxidation levels. Simultaneous treatment with 4-hydroxy-2,2,6,6-tetramethyl piperidinoxyl (Tempol), a membrane-permeable radical scavenger, completely eliminated the increases of phosphorylated MAP kinases and their upstream elements (Raf-1, Rac-1, ASK-1) as well as the increases of cardiac lipid peroxidation induced by the highest dose of ISO infusion. In chronically ISO-infused rats (3 mg/kg/day, s.c. for 10 days), cardiac hypertrophy developed with accompanying increases of collagen content, whereas cardiac phosphorylated MAP kinases returned to normal. Tempol treatment prevented increases of collagen accumulation and type I collagen mRNA without any significant reduction of cardiac mass enlargement induced by chronic ISO infusion. CONCLUSION: beta-Adrenoceptor stimulation provokes cardiac oxidative stress. In the acute phase of ISO infusion, ROS are important activators of cardiac MAP kinase cascades; while, in the chronic phase, ROS may participate in cardiac remodeling, especially in respect to wall stiffness, based on fibrogenesis.     

Protective effects of a combination of quercetin and vitamin E against cyclosporine A-induced oxidative stress and hepatotoxicity in rats.

Aim: Cyclosporine A (CsA) is the most widely used immunosuppressive drug in transplant surgery. It is able to generate reactive oxygen species (ROS) and cause lipid peroxidation (thiobarbituric acid-reacting substances [TBARS]), which will directly result in CsA hepatotoxicity. Methods: In this study, the potential of quercetin (Q) and vitamin E (E), in attenuating CsA-induced liver dysfunction in rats was investigated. Male Sprague-Dawley rats were divided into six groups and treated with either olive oil, ethanol + olive oil, CsA, CsA + E, CsA + Q, or CsA + E + Q for both 4 and 8 weeks. Hepatotoxicity was assessed by morphological alterations in tissue architecture and by reduced serum total protein and increased serum alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase. Results: The results indicated that CsA treatment increases TBARS and decreases activities of catalase (CAT) and glutathione peroxidase (GPx) in the rat liver. The co-administration of E and Q with CsA treatment improved both liver morphology changes and function. A combination of these antioxidants significantly reduced TBARS and increased CAT and GPx activities in the hepatic tissue. Conclusion: Our data demonstrates that E + Q plays a protective role against the imbalance elicited by CsA between the production of free radicals and antioxidant defence systems, and suggests that a combination of these two antioxidants may find clinical application where cellular damage is a consequence of ROS.     

Ecstasy produces left ventricular dysfunction and oxidative stress in rats

AIMS: Our aim was to determine whether the repeated, binge administration of 3,4-methylenedioxymethamphetamine (ecstasy; MDMA) produces structural and/or functional changes in the myocardium that are associated with oxidative stress. METHODS AND RESULTS: Echocardiography and pressure-volume conductance catheters were used to assess left ventricular (LV) structure and function in rats subjected to four ecstasy binges (9 mg/kg i.v. for 4 days, separated by a 10 day drug-free period). Hearts from treated and control rats were used for either biochemical and proteomic analysis or the isolation of adult LV myocytes. After the fourth binge, treated hearts showed eccentric LV dilation and diastolic dysfunction. Systolic function was not altered in vivo; however, the magnitude of the contractile responses to electrical stimulation was significantly smaller in myocytes from rats treated in vivo with ecstasy compared with myocytes from control rats. The magnitude of the peak increase in intracellular calcium (measured by Fura-2) was also significantly smaller in myocytes from ecstasy-treated vs. control rats. The relaxation kinetics of the intracellular calcium transients were significantly longer in myocytes from ecstasy-treated rats. Ecstasy significantly increased nitrotyrosine content in the left ventricle. Proteomic analysis revealed increased nitration of contractile proteins (troponin-T, tropomyosin alpha-1 chain, myosin light polypeptide, and myosin regulatory light chain), mitochondrial proteins (Ub-cytochrome-c reductase and ATP synthase), and sarcoplasmic reticulum calcium ATPase. CONCLUSION: The repeated binge administration of ecstasy produces eccentric LV dilation and dysfunction that is accompanied by oxidative stress. These functional responses may result from the redox modification of proteins involved in excitation-contraction coupling and/or mitochondrial energy production. Together, these results indicate that ecstasy has the potential to produce serious cardiac toxicity and ventricular dysfunction.     

Hepatic morphological changes and oxidative stress in chronic streptozotocin-diabetic rats

Oxidative stress (OS) is a biological entity quoted as responsible for several pathologies including diabetes. Diabetes mellitus (DM) has been also associated to human cirrhosis. The present work was designed to study the occurrence of OS as well as morphologic alterations in rat livers following induction of DM. Two groups of rats were used: Control and Diabetic. DM was induced in the second group by streptozotocin (STZ) in a single dose of 60 mg/kg, injected i.p. The occurrence of OS was determined in liver homogenates by measuring the hydroperoxide-initiated chemiluminescence and the activity of antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase). Liver sinusoids were morphometrically analyzed. In conclusion, livers from the diabetic group did not show evidence of the occurrence of OS, as it would be expected, but dilation of hepatic sinusoids was documented and it was significantly different from control group.     

Olmesartan improves endothelin-induced hypertension and oxidative stress in rats.

Recent studies have indicated that both endothelin (ET) and angiotensin (Ang) II stimulate oxidative stress, which contributes to the development of hypertension. Here, we examined the effects of Ang II type 1 (AT1) receptor blockade on reactive oxygen species (ROS) formation in ET-dependent hypertension. Chronic ET-1 infusion (2.5 pmol/kg/min, i.v., n=7) into rats for 14 days increased systolic blood pressure from 113+/-1 to 141+/-2 mmHg. ET-1-infused rats showed greater plasma renin activity (8.1+/-0.8 Ang I/ml/h), and greater Ang I (122+/-28 fmol/ml) and Ang II levels (94+/-13 fmol/ml) than vehicle (0.9% NaCl)-infused rats (3.1+/-0.6 Ang I/ml/h, 45+/-8 and 47+/-7 fmol/ml, respectively, n=6). Angiotensin converting enzyme and AT1 receptor expression in aortic tissues were similar between the vehicle- and ET-1-infused rats. Vascular superoxide anion (O2-) production and plasma thiobarbituric acid-reactive substance (TBARS) levels were greater in ET-1-infused rats (27+/-1 counts per minutes [CPM]/mg dry tissue weight and 8.9+/-0.8 micromol/l, respectively) than vehicle-infused rats (16+/-1 CPM/mg and 5.1+/-0.1 micromol/l, respectively). The ET-1-induced hypertension was prevented by simultaneous treatment with a new AT1 receptor antagonist, olmesartan (0.01% in chow, 117+/-5 mmHg, n =7), or hydralazine (15 mg/kg/day in drinking water, 118+/-4 mmHg, n=6). Olmesartan prevented ET-1-induced increases in vascular O2- production (15+/-1 CPM/mg) and plasma TBARS (5.0+/-0.1 micromol/l). Vascular O2- production and plasma TBARS were also decreased by hydralazine (21+/-1 CPM/mg and 7.0+/-0.3 micromol/l, respectively), but these levels were significantly higher than in vehicle-infused rats. These data suggest that ET-dependent hypertension is associated with augmentation of Ang II levels and ROS formation. The combined effects of the elevations in circulating ET-1 and Ang II, as well as the associated ROS production, may contribute to the development of hypertension induced by chronic ET-1 infusion.     

Evaluation of the effect of oxidative stress and vitamin E supplementation on renal function in rats with streptozotocin-induced Type 1 diabetes

We investigated the possible role of reactive oxygen species (ROS) on renal function in experimental diabetes.Materials and MethodsSeven groups of male rats were studied. Group I consisted of control animals. Diabetes was induced (by streptozotocin) in the animals in the other groups and they received either insulin or vitamin E (300 or 600 mg/kg), both insulin and vitamin E, or no treatment for 4 weeks. At the end of the study, blood pressure was measured and parameters of kidney function and oxidative stress were evaluated in serum and kidney tissue samples.ResultsDiabetic animals had higher blood pressures; increased serum glucose, urea, creatinine, cyclic guanosine monophosphate (cGMP); increased kidney tissue levels of malondialdehyde and inducible nitric oxide synthetase (iNOS); and reduced serum glutathione peroxidase when compared with control animals. Blood glucose levels in diabetic animals were controlled by insulin and not by any dose of vitamin E alone. However, all other measured parameters improved towards control levels with either insulin or vitamin E in either dose. An additive beneficial effect was observed on the levels of iNOS and cGMP when both forms of treatment were used in diabetic animals.ConclusionsWe conclude that ROS may play an important role in diabetes-induced nephropathy in this rat model. Vitamin E supplementation in addition to insulin can have additive protective effects against deterioration of renal function in this model.     

The effect of 1alpha,25(OH)2D3 vitamin over oxidative stress and biochemical parameters in rats where Type 1 diabetes is formed by streptozotocin

IntroductionThe 1α,25-dihydroxyvitamin D₃ [1α,25(OH)₂D₃] plays an essential role in mineral balance but has also been recognized as a powerful modulator of immune response. We aimed to examine the effect of the 1α,25(OH)₂D₃ treatment on insulin/c-peptide, catalase, superoxide dismutase (SOD), and blood glucose in rats that take streptozotocin (STZ).MethodsForty pieces of male rats of Albino family whose average weights were 261.00±07.62 g were used in the study. Rats were made diabetic by giving STZ of 40 mg/kg during 5 days through intraperitoneal path. Some of the diabetic group and nondiabetic group were received 1α,25(OH)₂D₃. The levels of SOD, insulin, c-peptide, glucose, SOD, and catalase were measured at the zero, second, fourth, and sixth weeks.ResultsErythrocyte SOD levels didn't show a significant difference at the end of the sixth week in all groups when compared to the beginning. While erythrocyte catalase levels didn't show a significant difference in nondiabetic control and nondiabetic with vitamin D, and diabetic with vitamin D groups at the end of sixth week when compared to the beginning, a significant measurement was made in diabetic without vitamin D group. Maximal insulinitis scoring values were observed in diabetic without vitamin D that didn't receive 1α,25(OH)₂D₃ treatment.ConclusionThe highness of insulin and c-peptide levels in the group that received treatment when compared to other groups and the lowness of oxidative markers such as SOD, catalase in this study can be explained by the fact that 1α,25(OH)₂D₃ treatment prevents the intervention of apoptosis mechanism.     

Comprehensive analysis of gene expression in Nicotiana tabacum leaves acclimated to oxidative stress

The molecular mechanisms by which plants acclimate to oxidative stress are poorly understood. To identify the processes involved in acclimation, we performed a comprehensive analysis of gene expression in Nicotiana tabacum leaves acclimated to oxidative stress. Combining mRNA differential display and cDNA array analysis, we estimated that at least 95 genes alter their expression in tobacco leaves acclimated to oxidative stress, of which 83% are induced and 17% repressed. Sequence analysis of 53 sequence tags revealed that, in addition to antioxidant genes, genes implicated in abiotic and biotic stress defenses, cellular protection and detoxification, energy and carbohydrate metabolism, de novo protein synthesis, and signal transduction showed altered expression. Expression of most of the genes was enhanced, except for genes associated with photosynthesis and light-regulated processes that were repressed. During acclimation, two distinct groups of coregulated genes ("early-" and "late-response" gene regulons) were observed, indicating the presence of at least two different gene induction pathways. These two gene regulons also showed differential expression patterns on an oxidative stress challenge. Expression of "late-response" genes was augmented in the acclimated leaf tissues, whereas expression of "early-response" genes was not. Together, our data suggest that acclimation to oxidative stress is a highly complex process associated with broad gene expression adjustments. Moreover, our data indicate that in addition to defense gene induction, sensitization of plants for potentiated gene expression might be an important factor in oxidative stress acclimation.