The effects of cyclosporine on antioxidant enzyme activities and malondialdehyde levels in rabbit hepatic tissues

Possible molecular mechanisms leading to cyclosporine-induced hepatotoxicity has not been cleared yet. Therefore, investigation of antioxidant status of hepatic tissues exposed to cyclosporine A (CsA) and of free radical involvement in the CsA-induced hepatotoxicity seems of importance. For this aim, 20 rabbits were used in the study. In each group (control, CsA, CsA plus vitamin and, vitamin only) there were 5 animals. CsA was given orally (25 mg/kg/day) for 10 days. Vitamins E (100 mg/kg/ day) and C (200 mg/kg/day) combination was injected intramuscularly. After 10th day, animals were killed, and livers were prepared for the enzymatic assays. Activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) and, malondialdehyde (MDA) levels were determined in the supernatant fractions. Lowered SOD, unchanged GSH-Px and, increased CAT activities and MDA levels were detected in hepatic tissues of rabbits treated with CsA as compared with controls. In the CsA plus vitamin group, SOD activity was found to be higher, GSH-Px and CAT activities unchanged and MDA levels lower than the CsA group. In the vitamin-treated group, all of the enzyme activities were higher than the controls but MDA levels were unchanged. Correlation analysis revealed some significant differences between the groups. Results suggest that cyclosporine impairs the antioxidant defense system and thus, leads to oxidant stress and peroxidation in rabbit hepatic tissues. It has been established that this process can be prevented by antioxidant vitamin supplementation.     

Efficacy of topotecan treatment on antioxidant enzymes and TBA-RS levels in submandibular glands of rabbits: an experimental study.

OBJECTIVE: The aim of this study was to investigate the effects of topotecan (Hycamtin), a topoisomerase I inhibiting anticancer agent, on antioxidant enzymes (SOD, CAT, and GSH-Px) and TBA-RS values of the submandibular glands of the rabbits. STUDY DESIGN AND SETTING: The study was conveyed in two groups (Group I, II) and control with a total of 24 rabbits. Eight rabbits in group I received intravenous (i.v.) topotecan (0.25 mg/kg once daily) for 3 days. Eight rabbits in group II received i.v. topotecan (0.5 mg/kg once daily) for 3 days. On the 15th day after administration of topotecan, submandibular glands were removed and levels of the SOD, CAT, and GSH-Px and the TBA-RS in the submandibular glands of the rabbits were examined. RESULTS: SOD, CAT, and GSH-Px values were significantly higher in high-dose topotecan group compared to control group (P < 0.05). SOD and TBA-RS values were significantly higher in high-dose topotecan group compared to low-dose topotecan group (P < 0.05). CONCLUSION: It was concluded that, to prevent the hazardous effects of oxygen free radicals due to topotecan, antioxidant enzymes SOD, CAT, and GSH-Px were increased. The higher levels of the TBA-RS values in group II showed that permanent damage was present because of high-dose topotecan administration in the submandibular glands of the rabbits.     

Effects of melatonin on lipid peroxidation and antioxidant enzymes in streptozotocin-induced diabetic rat testis

Aim:To examine the effects of melatonin treatment on lipid peroxidation(LPO)and the activities of antioxidantenzymes in the testicular tissue of streptozotocin(STZ)-induced diabetic rats.Methods:Twenty-six male rats wererandomly divided into three groups as follows:group Ⅰ,control,non-diabetic rats(n=9);group Ⅱ,STZ-induced,untreated diabetic rats(n = 8);group Ⅲ,STZ-induced,melatonin-treated(dose of 10 mg/kg-day)diabetic rats(n=9).Following 8-week melatonin treatment,all rats were anaesthetized and then were killed to remove testes from thescrotum.Results:As compared to group Ⅰ,in rat testicular tissues of group Ⅱ,increased levels of malondialdehyde(MDA)(P<0.01)and superoxide dismutase(SOD)(P<0.01)as well as decreased levels of catalase(CAT)(P<0.01)and glutathione peroxidase(GSH-Px)(P>0.05)were found.In centrast,as compared to group Ⅱ,in rat testiculartissues of group Ⅲ,levels of MDA decreased(but this decrease was not significant,P>0.05)and SOD(P<0.01)aswell as CAT(P<0.05)increased.GSH-Px was not influenced by any of the treatment.Melatonin did not signifi-cantly affect the elevated glucose concentration of diabetic group.At the end of the study,there was no significantdifference between the melatonin-treated group and the untreated group by means of body and testicular weight.Conclusion:Diabetes mellitus increases oxidative stress and melatonin inhibits lipid peroxidation and might regulatethe activities of antioxidant enzymes of diabetic rat testes.(Asian J Androl 2006 Sep;8:595-600)     

Impact of polychlorinated biphenyl （Aroclor 1254） and vitamin C on antioxidant system of rat ventral prostate

Aim: To evaluate the effect of polychlorinated biphenyls (PCB) and vitamin C on ventral prostatic antioxidant system in adult male rats. Methods: A group of 20 adult male rats were administered ip Aroclor 1254 in corn oil at a dose of 2 mg·kg-1·day-1 for 30 days. Ten control rats were administered only the vehicle. After 30 days the treated rats were divided at random into 2 sub-groups of 10 animals each. One sub-group received vitamin C at a dose of 500 mg·kg-1·day-1 for 10 days. The other group was maintained as Aroclor 1254 control. Twenty-four hours after the last treatment the rats were killed by decapitation. Ventral prostatic homogenate was prepared and used for the estimation of enzymatic antioxidants, including superoxide dismutase (SOD), catalase (CAT) and glutathione-S-transferase (GST) and hydrogen peroxide (H2O2), lipid peroxidation (LPO) and prostatic acid phosphatase. The serum levels of total T3, total T4, TSH, testosterone and estradiol were also assayed. Results: The body weight and     

Protective effects of hyperoxygenated solution preconditioning on intestinal ischemia-reperfusion injury in rabbits

BACKGROUND: The aim of this study was to investigate the protective effects of hyperoxygenated solution (HOS) preconditioning on intestinal ischemia-reperfusion (IR) injury in rabbits. MATERIALS AND METHODS: Thirty-two rabbits were randomly divided into four groups as follows: (1) control group in which sham operation was performed (Sham group); (2) sham operation and HOS treatment group (sham+H group); (3) ischemia-reperfusion group (IR group); (4) ischemia-reperfusion and HOS treatment group (H group). Intestinal IR model was produced by clamping superior mesenteric artery with an atraumatic vascular clamp for 1 h, followed by reperfusion for 2 h. Animals in H group received intravenous HOS infusion (20 mL/kg) every day for 5 days before ischemia-reperfusion; animals in the sham+H group received the same amount of HOS before sham operation, and animals in IR group received the same amount of normal saline in the same way. At the end of reperfusion, histopathological changes of intestine were observed, and malondialdehyde (MDA) levels, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities in intestinal tissues were also detected. Intestinal barrier function was assessed by blood d-lactate levels and bacterial translocation (BT). RESULTS: The H group showed significantly lower MDA levels and higher activities of SOD, CAT, and GSH-Px in the intestinal tissue compared with the IR group. Furthermore, the mean d-lactate levels and incidence of BT in the H group were significantly lower than those in the IR group. Histopathological analysis also indicated that there were significant histological improvements in the H group compared with the IR group. CONCLUSIONS: HOS preconditioning at an appropriate dose ameliorates the deleterious changes in intestinal mucosal injury and barrier function associated with IR by effectively preventing a decrease in the intestinal antioxidant defense system, which is another simple and effective measure to protect intestine from IR injury.     

Beneficial effects of chrysin on the reproductive system of adult male rats

In this study, the beneficial effect of chrysin, a natural flavonoid currently under investigation due to its important biological activities, on reproductive system of rats was investigated. Rats (n = 16) were divided randomly into two equal groups. Rats in control group were given corn oil as carrier. Chrysin was orally administered at the dose of 50 mg kg(-1) per day by gavages, and it was dissolved in corn oil for 60 days. Tissue thiobarbituric acid reactive substances (TBARS) and glutathione (GSH) levels, antioxidant enzyme activity (CAT, SOD and GSH-Px), sperm parameters (motility, concentration and abnormal sperm rate), reproductive organ weight (testes, epididymis, vesicula seminalis, prostate) and serum testosterone levels were determined in the rats. Our results indicated that chrysin significantly increased GSH, CAT, GSH-Px and CuZn-SOD levels, but did not change the formation of TBARS significantly. In addition, sperm motility, sperm concentration and serum testosterone levels significantly increased, whereas abnormal sperm rate significantly decreased with chrysin treatment. In conclusion, it is suggested that treatment with chrysin can positively affect the reproductive system in rats, and it can be used for the treatment of male infertility.     

The protective effects of melatonin and vitamin E against renal ischemia-reperfusion injury in rats

Reactive oxygen species (ROS) were shown to contribute to the cellular damage induced by ischemia-reperfusion. The purpose of this study was to investigate and compare the efficiency of melatonin and vitamin E in the reduction of injury induced by ROS in a rat model of renal ischemia-reperfusion. Twenty-four Wistar-albino rats were divided into four groups. Rats in the Sham group were given saline 1 mL/kg, intraperitoneally (ip) 72 h, 48 h, 24 h, and 30 min before the sham operation. Rats in ischemia-reperfusion (IR), IR+Melatonin, and IR+Vitamin E groups were given saline (1 mL/kg), melatonin (10 mg/kg), and vitamin E (100 mg/kg) ip, respectively, 72 h, 48 h, 24 h, and 30 min before the ischemia for 60 min, followed by reperfusion for 60 min. The blood samples and kidney tissues of the rats were taken under anesthesia. Ischemia-reperfusion significantly increased urea, creatinine, and malondialdehyde (MDA) levels, and decreased superoxide dismutase (SOD) and catalase (CAT) activities. Histopathological findings of the IR group confirmed that there was renal impairment by cast formation and tubular necrosis in the tubular epithelium. In the IR+Melatonin group, while MDA levels significantly decreased, SOD activities increased. In the IR+Melatonin group, the level of tubular necrosis and cast formation are significantly decreased than those seen in the ischemia-reperfusion group. Melatonin in particular was effective to reverse hot ischemia of kidney by its antioxidant effects. These results may indicate that melatonin pretreatment protects against functional, biochemical, and morphological damage better than vitamin E in renal ischemia-reperfusion injury.     

The Protective Effects of Melatonin and Vitamin E against Renal Ischemia-Reperfusion Injury in Rats

Reactive oxygen species (ROS) were shown to contribute to the cellular damage induced by ischemia-reperfusion. The purpose of this study was to investigate and compare the efficiency of melatonin and vitamin E in the reduction of injury induced by ROS in a rat model of renal ischemia-reperfusion. Twenty-four Wistar-albino rats were divided into four groups. Rats in the Sham group were given saline 1 mL/kg, intraperitoneally (ip) 72 h, 48 h, 24 h, and 30 min before the sham operation. Rats in ischemia-reperfusion (IR), IR+Melatonin, and IR+Vitamin E groups were given saline (1 mL/kg), melatonin (10 mg/kg), and vitamin E (100 mg/kg) ip, respectively, 72 h, 48 h, 24 h, and 30 min before the ischemia for 60 min, followed by reperfusion for 60 min. The blood samples and kidney tissues of the rats were taken under anesthesia. Ischemia-reperfusion significantly increased urea, creatinine, and malondialdehyde (MDA) levels, and decreased superoxide dismutase (SOD) and catalase (CAT) activities. Histopathological findings of the IR group confirmed that there was renal impairment by cast formation and tubular necrosis in the tubular epithelium. In the IR+Melatonin group, while MDA levels significantly decreased, SOD activities increased. In the IR+Melatonin group, the level of tubular necrosis and cast formation are significantly decreased than those seen in the ischemia-reperfusion group. Melatonin in particular was effective to reverse hot ischemia of kidney by its antioxidant effects. These results may indicate that melatonin pretreatment protects against functional, biochemical, and morphological damage better than vitamin E in renal ischemia-reperfusion injury.     

Impaired antioxidant defence in guinea pig heart tissues treated with halothane

Purpose

To investigate the effects of halothane and halothane plus vitamin E treatment on myocardial free radical metabolism in guinea pigs.

Methods

Four groups of seven animals were studied; control, halothane, halothane plus vitamin E and vitamin E groups. In the halothane group, halothane 1.5% in oxygen was given for 90 min over three days. In the halothane plus vitamin E group, 300 rng · kg^?1 · day^?1 vitamin Eim was started three days before the first halothane treatment and continued for three days. Following sacrifice, the hearts were assayed for superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) and malondialdehyde (MDA) level was determined. Electron spin resonance (ESR) analysis and electron microscopy (EM) were also performed.

Results

In the halothane group, SOD activities and MDA concentrations were increased compared with control and GSH-Px and CAT activities were decreased. In the halothane plus vitamin E group, there were no differences in enzyme activity compared with halothane alone but the MDA level was decreased. In the vitamin E group, enzyme activities were increased compared with control. Mainly the CF₃CHCl radical was identified by ESR analysis in heart tissues exposed to halothane and the concentration of this radical was reduced by vitamin E. Electron microscopy showed cytoplasmic vacuolisation and dilation in sarcoplasmic reticulum in the heart tissues exposed to halothane: both were prevented by vitamin E.

Conclusion

Although halothane causes impairment in enzymatic antioxidant defence potential, due to lowered GSH-Px and CAT activity, and accelerates peroxidative reactions in the tissues affected, no subcellular damage occurred. Vitamin E may protect tissues against free radical attack by scavenging toxic free radicals formed in heart tissue during halothane anaesthesia.     

酒精对大鼠前列腺抗氧化酶活性和脂质过氧化的影响

目的 探讨酒精对大鼠前列腺组织抗氧化酶活性和脂质过氧化水平的影响。方法 40只成年健康SD雄性大鼠随机均分为对照组、低剂量组、中剂量组和高剂量组，分别用50．0％、25．0％、12．5％的乙醇溶液和蒸馏水按10．0ml／kg每晚灌胃1次持续60d后，观察酒精毒染模型大鼠前列腺组织的形态结构的变化；用化学比色法测定前列腺组织中超氧化物岐化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-Px）、丙二醛（MDA）和前列腺酸性磷酸酶（PAP）的水平。结果 随着酒精剂量的增加，SOD、CAT、GSH-Px活力和PAP含量呈先升高后下降的趋势，MDA含量和前列腺相对重量分别呈现上升和下降趋势，前列腺组织馆牛棼缩。结论 长期过量饮洒可导致大鼠前列腺绸织结构和功能异常，氧化应激在其中发挥了重要作用。     

Antioxidative status and lipid peroxidation in kidney tissue of rats fed with vitamin B6-deficient diet

Introduction: The aim of this study was to evaluate lipid peroxidation (LP) and free radical scavenging enzyme activities in kidney tissue of vitamin B₆-deficient rats. Material and Methods: The rats were divided into control and vitamin B₆-deficient groups. After 4 weeks of feeding, animals in all groups were anesthetized by thiopental sodium (50 mg/kg). Thoraces were opened, 2 mL blood samples were taken from aortas, then the rats were killed by cervical dislocation, and kidney tissues were removed. Biochemical measurements in kidney tissue were carried out using a spectrophotometer. Results: Total superoxide scavenger activity (TSSA), nonenzymatic superoxide scavenger activity (NSSA), superoxide dismutase (SOD) activities, and antioxidant potential (AOP) values in the vitamin B₆-deficient group were significantly lower than those of the control group, whereas glutathione peroxidase (GSH-Px), glutathione reductase (GRD), glutathione-S-transferase (GST) activities, and malondialdehyde (MDA) level were significantly higher than those of the control group (p < 0.05). Discussion: The results show that vitamin B₆ deficiency causes an attenuation in antioxidant defense system and an increase in oxidative stress in kidney tissue of rats.     

Quercetin prevents 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced testicular damage in rats

The protective effect of quercetin on 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced testicular damage in rats was investigated. Twenty-two rats were equally divided into four groups; first group was kept as control and given corn oil as carrier. In second group, TCDD was orally administered at the dose of 2 μ (kg week)(-1) for 60 days. In third group, quercetin was orally administered at the dose of 20 mg (kg day)(-1) by gavages, and in fourth group TCDD and quercetin were given together at the same doses. Although TCDD increased the formation of thiobarbituric acid reactive substances (TBARS) significantly, it caused a significant decline in the levels of glutathione (GSH), catalase (CAT), GSH-Px and CuZn-Superoxide Dismutase (CuZn-SOD) in rats. In contrast, quercetin significantly increased the GSH, CAT, GSH-Px and CuZn-SOD levels but decreased the formation of TBARS. In addition, sperm motility, sperm concentration and serum testosterone levels were significantly decreased but abnormal sperm rate and testicular damage were increased with TCDD treatment. However, these effects of TCDD on sperm parameters, histological changes and hormone levels were eliminated by quercetin treatment. Our results show that administration of TCDD induces testicular damage (oxidative stress, testes tissue damage, serum hormone level and sperm parameters), and quercetin prevents TCDD-induced testicular damage in rats. Thus, quercetin may be useful for the prevention and treatment of TCDD-induced testicular damage.     

Effects of endurance training on antioxidant defense mechanisms and lipid peroxidation in testis of rats

Male rats were equally divided into trained rest (TR), trained exhaustive exercise (TE), untrained rest (UR), and untrained exhaustive exercise (UE). Endurance training consisted of treadmill running for 1.5 h/d, 5 days a week for 8 weeks reaching the speed of 2.1 km/h at the fortieth week. For acute exhaustive exercise, graded treadmill running was conducted reaching the speed of 2.1 km/h at 95th min, 10% uphill, continued until exhaustion. Testicular tissue malondialdehyde (MDA), antioxidant potential (AOP) levels, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione-S-transferase (GST), glutathione reductase (GR) and catalase (CAT) activities were determined. There was a slight decrease, but not significant, in the SOD activity in UE group compared to TE and TR groups. Activity of GSH-Px decreased in the UE group compared to UR, TR and TE groups. Acute exhaustive exercise did not affect testicular tissue GSH-Px activity in trained rats. Testicular tissue GST activity of the UE group was similar to TE group, but lower than UR and TR groups. In UE group, testicular tissue AOP values were lower than UR, TR and TE groups. The oxidative effects of acute exhaustive exercise on the rat testis decreased with endurance training. Endurance training prevents oxidative injuries by eliminating oxygen radicals and inhibiting lipid peroxidation via preventing decreases in antioxidant enzyme activities.     

Renal antioxidant status in rats with hypertension induced by N sup omega nitro-L-arginine methyl ester

Nitric oxide (NO) has a role in the etiopathogenesis of hypertension. Relaxation of vascular smooth muscles is failed when NO production is reduced leading to increased vascular peripheral resistance. N sup omega nitro-L-arginine methyl ester (L-NAME) is one of the inhibitors of NO production. The aim of this study was to investigate oxidant-antioxidant systems of renal tissue in rats with hypertension induced by L-NAME. Rats were divided into three groups: control group and study groups treated with 100 or 500 mg/l L-NAME in drinking water for 15 days. The activities of catalase (CAT), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD), and the levels of malondialdehyde (MDA) and NO were studied in the renal tissue after hypertension induction. Arterial blood pressure was increased in both L- NAME groups. CAT activity of 500-mg L-NAME group was higher than control. GSH-Px activity of 500-mg L-NAME group was decreased compared with 100-mg ones. NO level was lower in 500-mg L-NAME group than control. MDA levels in both L-NAME groups were decreased compared with control. In conclusion, hypertension was induced with oral L-NAME treatment. Increased CAT activity was compensated with decreased GSH-Px activity in 500-mg L-NAME group. Both study groups were protected from lipid peroxidation with NO inhibition.     

The effect of dehydroepiandrosterone on renal ischemia-reperfusion-induced oxidative stress in rabbits

Reactive oxygen species (ROS) can play an important role in the pathogenesis of ischemia-reperfusion (I/R) injury. Dehydroepiandrosterone (DHEA) is one of the hormones secreted from adrenal glands, and in some studies it has been shown that DHEA has antioxidant properties. This experimental study was designed to determine the effect of DHEA on I/R-induced oxidative stress in rabbit kidney. Twenty-one rabbits were divided into three groups. Rabbits were subjected to 60 min of left renal pedicle occlusion followed by 24 h of reperfusion. DHEA (50 mg/kg) (I/R + DHEA group) or equal volume of vehicle (I/R group) was administered 3 h prior to ischemia. The control group received only laparotomy without I/R, DHEA or vehicle. At the end of the reperfusion periods, rabbits were decapitated. Renal tissues were taken for determination of malondialdehyde (MDA) levels as an indicator of lipid peroxidation and superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) activities as antioxidant enzymes. In the I/R group, while renal SOD and CAT activities were significantly lower, MDA levels were significantly higher than in the I/R + DHEA group and controls. In the I/R + DHEA group, enzyme activities and MDA levels were similar to the controls. There was no significant difference in terms of renal GPX activity among the groups. DHEA may have a beneficial effect on renal tissue against oxidative damage due to I/R by preventing decreases in some antioxidant enzyme activities.     

Curcumin protects against ischemia/reperfusion injury in rat kidneys

OBJECTIVES: Renal ischemia followed by reperfusion leads to acute renal failure in both native kidneys and renal allograft. We investigated the effect of curcumin on ischemia-reperfusion (I/R) injury and the antioxidant effects of curcumin in rats. METHODS: Thirty rats were randomly divided into five experimental groups (control, sham, curcumin, I/R and I/R+curcumin, n=6 each). Curcumin was administered (200 mg kg(-1)) orally to curcumin and I/R+curcumin groups for 7 days. Then, the rats were subjected to bilateral renal ischemia for 45 min and followed by reperfusion for 24 h. All rats were killed and kidney function tests, serum and tissue nitric oxide (NO), protein carbonyl (PC), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels were determined. Histopathological examinations were also performed. RESULTS: Curcumin significantly improved the urea and cystatin C levels in I/R+curcumin group compared to I/R group (p<0.05). Reduction of serum GSH-Px was significantly improved by curcumin (p<0.001), but SOD enzyme activity did not alter (p>0.05). Treatment with curcumin also resulted in significant reduction in serum and tissue MDA, NO and PC and for tissue that were increased by renal I/R injury (p<0.001 for serum and p<0.05 for tissue, respectively). In histological examination, the rats treated with curcumin had nearly normal morphology of the kidney. CONCLUSIONS: Based on our results, it can be concluded that curcumin protects the kidneys against I/R injury via its antioxidant effects.     

右美托咪定对大鼠局灶性脑缺血-再灌注损伤后抗氧化能力的影响

目的观察右美托咪定预先处理对大鼠局灶性脑缺血-再灌注损伤后抗氧化能力的影响。方法健康雄性SD大鼠42只,体重250~280g,随机分为假手术组(Sham组)、缺血-再灌注组(IR组)和右美托咪定组(DEX组),每组14只。采用大脑中动脉线栓法制作大鼠局灶性脑缺血-再灌注损伤模型,具体方法为线栓法栓塞大脑中动脉2h后恢复再灌注。Sham组仅分离血管,不留置线栓;于大脑中动脉栓塞前30 min DEX组给予腹腔注射盐酸右美托咪定注射液100μg/kg(4μg/ml),IR组腹腔注射等量的生理盐水。三组均于再灌注24h后取8只大鼠进行神经功能评分,测定脑梗死体积;剩余6只大鼠取脑组织检测超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSHPX)、谷胱甘肽还原酶(GR)和过氧化氢酶(CAT)活性。结果 IR组和DEX组神经功能评分明显高于Sham组,脑梗死体积明显大于Sham组,SOD、GSH-PX、GR、CAT活性明显低于Sham组(P0.05);DEX组大鼠神经功能评分明显低于IR组,脑梗死体积明显小于IR组,SOD、GSH-PX、GR、CAT活性明显高于IR组(P0.05)。结论右美托咪定有保护内源性抗氧化酶活性作用,可能有助于减轻大鼠脑缺血-再灌注损伤。     

Glucocorticoid activates glomerular antioxidant enzymes and protects glomeruli from oxidant injuries

We examined the effect of glucocorticoid on intrinsic glomerular antioxidant enzyme (AOE) activities. Munich-Wistar rats were treated with daily i.p. injection of vehicle or methylprednisolone [MP, 15 mg/kg body wt, (MP15)] either for three days or nine days. Glomeruli isolated from rats given MP15 had significantly higher activities of total (T-) and manganese (Mn-) superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase than vehicle-treated rats (P less than 0.05). MP15-treated rats were subjected to intrarenal arterial infusion of hydrogen peroxide (35 mumol over 1 hr). Values for urinary protein excretion rate (UprV) after hydrogen peroxide infusion were markedly lower in rats pretreated with MP15 for both three days and nine days than in untreated rats (109 +/- 18 and 55 +/- 24 vs. 416 +/- 73 micrograms/min, respectively, both P less than 0.005). To test whether the same therapeutic intervention attenuates reactive oxygen species (ROS)-mediated glomerular injury in another model, rats given a single i.v. dose of puromycin aminonucleoside (PAN) (50 mg/kg body wt) were treated with daily i.p. injection of vehicle or MP15. Two days after PAN administration, when compared to vehicle-treated controls, PAN rats given MP15 had significantly higher activities of Mn-SOD, GSH-Px and catalase. After eight days of PAN injection, T- and Mn-SOD activities were, likewise, significantly higher in MP15- than vehicle-treated PAN rats. PAN rats given MP15 also had substantially less proteinuria, compared to PAN rats given vehicle alone, UprV averaging 32.3 +/- 9.4 versus 159.0 +/- 13.8 mg/24 hr (P less than 0.05). Elevated glomerular malondialdehyde (MDA) level characteristic of PAN rats was absent in rats treated with MP15. Moreover, epithelial foot process fusion and cell vacuolization seen in vehicle-treated PAN rats were markedly attenuated in MP15-treated PAN rats. These data indicate that the mechanism for therapeutic effect of glucocorticoids on ROS-mediated renal injuries includes an enhancement of endogenous glomerular AOE activities, which attenuates lipid peroxidation of glomerular tissue.     

Allopurinol prevents erythrocyte deformability impairing but not the hematological alterations after limb ischemia-reperfusion in rats.

The measurement of red blood cell deformability provides a possible method for detecting the effect of ischemia-reperfusion on erythrocytes. In our study the effect of 1-h ischemia-reperfusion with or without allopurinol pretreatment on hematological parameters and red blood cell deformability was investigated in a follow-up experiment of 26 male CD outbred rats that were subjected to unilateral hind-limb ischemia by microvascular clips on femoral vessels for 1 h (IR, n = 6), some rats received allopurinol pretreatment under the same conditions (50 mg/kg, AP + IR, n = 8), others were subjected to sham operation (n = 6), and the rest of animals served as control (n = 6). Measurement of erythrocyte deformability using a bulk filtrometer with special setting of cell suspension hematocrit (1%), and determination of hematological parameters were performed daily for one week. In the IR group, relative cell transit time increased significantly on postoperative days 1 and 2, which was not observed in the other groups. Settings for the measurement of erythrocyte deformability by reducing the blood sample volume gave the possibility of monitoring the resulting changes in rats. Mean corpuscular volume and hemoglobin, platelet count, and platelet volume were higher in the IR and AP + IR groups than in the other groups. In summary, short-term ischemia and reperfusion induced lower red blood cell deformability in the early postoperative period, which could be prevented by allopurinol pretreatment.     

Protective effects of thymoquinone against apoptosis and oxidative stress by arsenic in rat kidney

We aimed to investigate the protective role of thymoquinone (TQ) by targeting its antiapoptotic and antioxidant properties against kidney damage induced by arsenic in rats. We have used the 24 male Sprague-Dawley rats. Rats were divided into three groups. Physiological serum in 10?mL/kg dose as intragastric was given to the control group. Sodium arsenite (10?mg/kg, intragastric by gavage for fifteen days) was given to the arsenic group. Sodium arsenite (10?mg/kg, intragastric by gavage for fifteen days) and TQ (10?mg/kg, intragastric by gavage for 15 days) was given to the arsenic?+?TQ group. After 15 days, the animals’ kidneys were taken theirs, then we have performed histological and apoptotic assessment. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzyme activities and malondialdehyde (MDA) levels have examined as the oxidative stress parameters. We have determined the levels of arsenic. Increased renal injury and apoptotic cells have been detected in the arsenic group. Degenerative changes in the arsenic?+?TQ group were diminished. Although the MDA levels were augmented in the arsenic group, SOD, CAT and GSH-Px enzyme activities were lessened than the other groups. Our findings suggest that TQ may impede the oxidative stress, the cells have been damaged and also the generation of apoptotic cells arisen from arsenic. TQ plays a protective role against arsenic-induced toxicity in kidney and may potentially be used as a remedial agent.