Age-related changes of antioxidant enzyme activities, glutathione status and lipid peroxidation in rat erythrocytes after heat stress

The aim of this study was to determine whether exposure to heat stress would lead to oxidative stress and whether this effect varied with different exposure periods. We kept 1-, 6- and 12-month-old male Wistar rats at an ambient temperature of either 22 degrees C or 40 degrees C for 3 and 7 days and measured glucose-6-phosphate dehydrogenase (G-6-PD), Cu,Zn-superoxide dismutase (Cu,Zn-SOD), catalase (CAT), selenium-dependent glutathione peroxidase (Se-GSH-Px) and glutathione-S-transferase (GST) activities and levels of thiobarbituric acid-reactive substances (TBARS), reduced glutathione (GSH) and oxidized glutathione (GSSG) in erythrocytes and determined GSH/GSSG ratio, total glutathione and the redox index. G-6-PD and CAT activities were found to be significantly increased in 1- and 6-month-old rats after 3 and 7 days of heat stress, but G-6-PD activities decreased in 12-month-old rats. Cu, Zn-SOD activity decreased in 1-month-old rats after heat stress, whereas it increased in 6- and 12-month-old rats. GST activity increased in all groups. GSH and total GSH levels and GSH/GSSG ratios decreased in 1- and 6-month-old rats but they increased in 12-month-old rats after heat stress. GSSG levels increased in 1- and 6-month-old rats but decreased in 12-month-old rats after heat stress. TBARS levels increased in all groups. Seven days of stress is more effective in altering enzyme activities and levels of GSH, GSSG and TBARS. When the effects of both heat stress and aging were examined together, it was interesting to note that they mostly influenced G-6-PD activity.     

Beneficial effect of combined administration of some naturally occurring antioxidants (vitamins) and thiol chelators in the treatment of chronic lead intoxication

Ameliorative effects of few naturally occurring antioxidants like ascorbic acid (vitamin C), alpha-tocopherol (vitamin E) either alone or in combination with meso-2,3-dimercaptosuccinic acid (DMSA) or monoisoamyl DMSA (MiADMSA), on parameters indicative of oxidative stress in the liver, kidney, brain and blood of lead-exposed rats were studied. Male Wistar rats were exposed to 0.1% lead acetate in drinking water for 3 months and treated thereafter with DMSA or its analogue MiADMSA (50 mg/kg, intraperitoneally), either individually or in combination with vitamin E (5 mg/kg, intramuscularly) or vitamin C (25 mg/kg, orally) once daily for 5 days. The effects of these treatments in influencing the lead-induced alterations in haem synthesis pathway, hepatic, renal and brain oxidative stress and lead concentration from the soft tissues were investigated. Exposure to lead produced a significant inhibition of delta-aminolevulinic acid dehydratase (ALAD) activity from 8.44+/-0.26 in control animals to 1.76+/-0.32 in lead control, reduction in glutathione (GSH) from 3.56+/-0.14 to 2.57+/-0.25 and an increase in zinc protoporphyrin level from 62.0+/-3.9 to 170+/-10.7 in blood, suggesting altered haem synthesis pathway. Both the thiol chelators and the two vitamins were able to increase blood ALAD activity towards normal, however, GSH level responded favorably only to the two thiol chelators. The most prominent effect on blood ALAD activity was, however, observed when MiADMSA was co-administered with vitamin C (7.51+/-0.17). Lead exposure produced a significant depletion of hepatic GSH from 4.59+/-0.78 in control animals to 2.27+/-0.47 in lead controls and catalase activity from 100+/-3.4 to 22.1+/-0.25, while oxidized glutathione (GSSG; 0.34+/-0.05 to 2.05+/-0.25), thiobarbituric acid reactive substance (TBARS; 1.70+/-0.45 to 5.22+/-0.50) and glutathione peroxidase (GPx) levels (3.41+/-0.09 to 6.17+/-0.65) increased significantly, pointing to hepatic oxidative stress. Altered, reduced and oxidized GSH levels showed significant recovery after MiADMSA and DMSA administration while, vitamins E and C were effective in reducing GSSG and TBARS levels and increasing catalase activity. Administration of MiADMSA alone and the combined administration of vitamin C along with DMSA and MiADMSA were most effective in increasing hepatic GSH levels to 4.88+/-0.14, 4.09+/-0.12 and 4.30+/-0.06, respectively. Hepatic catalase also reached near normal level in animals co-administered vitamin C with DMSA or MiADMSA (82.5+/-4.5 and 84.2+/-3.5, respectively). Combined treatments with vitamins and the thiol chelators were also able to effectively reduce lead-induced decrease in renal catalase activity and increase in TBARS and GPx level. Combination therapy, however, was unable to provide an effective reversal in the altered parameters indicative of oxidative stress in different brain regions, except in catalase activity. The result also suggests a beneficial role of vitamin E when administered along with the thiol chelators (particularly with MiADMSA) in reducing body lead burden. Blood lead concentration was reduced from 13.3+/-0.11 in lead control to 0.3+/-0.01 in MiADMSA plus vitamin E-treated rats. Liver and kidney lead concentration also showed a most prominent decrease in MiADMSA plus vitamin E co-administered rats (5.29+/-0.16 to 0.63+/-0.02 and 14.1+/-0.21 to 1.51+/-0.13 in liver and kidney, respectively). These results thus suggest that vitamin C administration during chelation with DMSA/MiADMSA was significantly beneficial in reducing oxidative stress however, it had little or no additive effect on the depletion of lead compared with the effect of chelators alone. Thus, the co-administration of vitamin E during chelation treatment with DMSA or MiADMSA could be recommended for achieving optimum effects of chelation therapy.     

Effects of leptin on oxidative stress in healthy and Streptozotocin-induced diabetic rats

Aims/hypothesis It is generally accepted that oxidative stress is responsible for etiology and complications of diabetes. During uncontrolled Type 1 diabetes, plasma leptin levels rapidly fall. However, it is not known whether diabetes-induced hypoleptinemia has any role in oxidative stress related to uncontrolled Type I diabetes. The present study was designed to examine the effects of leptin treatment on plasma lipid peroxidation and reduced glutathion of normal and streptozotocin(STZ)-induced diabetic rats. Methods Diabetes was induced by single injection of Streptozotocin (55 mg/kg bw). One week after induction of diabetes, rats began 5-day treatment protocol of leptin injections of (0.1 mg/kg bw i.p.) or same volume vehicle. At the end of the 5th day, rats were sacrificed by cardiac puncture under anesthesia and their plasma was taken for plasma leptin, malondialdehyde, and reduced glutathione measurements. Results Plasma leptin levels decreased in STZ-induced diabetic rats while plasma glucose, TBARS, and GSH levels increased. Plasma leptin levels were not affected with leptin treatment in both diabetic and non-diabetic rats. The elevation in plasma TBARS associated with STZ diabetes decreased with leptin treatment. Leptin also increased plasma GSH levels in diabetic rats. In non-diabetic rats, treatment with leptin did not change plasma TBARS and GSH levels. Conclusions/interpretations In conclusion, leptin treatment is able to attenuate lipid peroxidation in STZ-diabetic rats, in the onset of diabetes, by increasing the GSH levels without affecting hyperglycemia and hypoleptinemia.     

A single exposure of rats to water-immersion restraint stress induces oxidative stress more severely in the thymus than in the spleen

Abstract

Objectives

We examined whether a single exposure of rats to water-immersion restraint stress (WIRS) induces oxidative stress in the thymus and spleen.

Methods

Vitamin E, ascorbic acid, reduced glutathione (GSH), and lipid peroxide (LPO) were assayed in the thymus and spleen of rats with and without 6 hours of WIRS.

Results

In unstressed rats, vitamin E, ascorbic acid, GSH, and LPO levels were higher in the thymus than in the spleen. Thymic ascorbic acid level was lower in stressed rats than in unstressed rats. Splenic ascorbic acid level was similar in both groups. Thymic and splenic GSH levels were lower in stressed rats than in unstressed rats but the reduced amount of GSH was lower in the spleen than in the thymus. Thymic vitamin E level was lower in stressed than in unstressed rats. Splenic vitamin E level was higher in stressed rats than in unstressed rats. Thymic and splenic LPO levels were higher in stressed rats than in unstressed rats but the increased amount of LPO was higher in the thymus than in the spleen.

Conclusion

It is indicated that a single expose of rats to WIRS induces oxidative stress more severely in the thymus than in the spleen.     

Impact of Hemidesmus indicus R.Br. extract on ethanol-mediated oxidative damage in rat kidney

The antioxidant effect of the ethanolic extract of Hemidesmus indicus R.Br. root (EHI), an indigenous Ayurvedic medicinal plant in India, was studied in rats with ethanol-induced nephrotoxicity. Administering 5 g/kg body weight/day of ethanol for 60 days to male Wistar rats resulted in significantly elevated levels of serum urea, creatinine and uric acid as well as kidney thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH) and conjugated dienes (CD) as compared to those of the experimental control rats. Decreased levels of kidney superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), vitamin C and vitamin E were also observed on alcohol administration as compared with those of the experimental control rats. EHI was administered at a dose of 500 mg/kg body weight/day for the last 30 days of the experiment to rats with ethanol-induced kidney injury, which significantly decreased the levels of serum urea, uric acid and creatinine as well as kidney TBARS, LOOH and CD and significantly elevated the activities of SOD, CAT, GPx, GSH, vitamin C and vitamin E in kidney as compared to that of untreated ethanol-administered rats. Histopathological observations also correlated with the biochemical parameters. Thus, the data indicate that treatment with EHI offers protection against free radical-mediated oxidative stress in kidney of animals with ethanol-induced nephrotoxicity.     

Exercise training restores oxidative stress and nitric oxide synthases in the rostral ventrolateral medulla of renovascular hypertensive rats

Abstract

We hypothesize that exercise training (EX) reverses the level of nitric oxide (NO) and oxidative stress into rostral ventrolateral medulla (RVLM) of renovascular hypertensive rats (two kidneys, one clip - 2K1C). Microinjections of L-arginine (5 nmol), L-NAME (10 nmol), or saline (100 nl) were made into RVLM of 2K1C and normotensive (SHAM) rats sedentary (SED) or subjected to swimming for 4 weeks. mRNA expression (by qRT-PCR) of nitric oxide synthases isoforms (nNOS, eNOS, and iNOS), manganese superoxide dismutase (MnSOD), copper and zinc superoxide (Cu/ZnSOD), catalase (CAT), NADPH oxidase subunit p22^phox, concentration of thiobarbituric acid-reactive substances (TBARS), and CAT activity into RVLM were evaluated. The mean arterial pressure was reduced in 2K1C EX compared with that in 2K1C SED rats. L-arginine into RVLM induced hypertensive effect in 2K1C and SHAM SED rats, while L-NAME prevented hypertensive effect only in SHAM-SED. EX reduced hypertensive effect of L-arginine in SHAM and 2K1C rats. mRNA expression of NOS isoforms, p22^phox, and concentration of TBARS were increased while CAT and Cu/ZnSOD expression and CAT activity decreased into RVLM of 2K1C-SED compared with SHAM-SED rats. Additionally, EX reversed mRNA expression of CAT and NOS isoforms, concentration of TBARS, and CAT activity into RVLM of 2K1C-EX rats. These data suggest that the levels of NOS and oxidative stress into RVLM are important to determine the level of hypertension. Furthermore, EX can restore the blood pressure by reversing the levels of NOS and CAT expression, and reducing TBARS concentration into RVLM for the physiological state.     

Impact of Hemidesmus indicus R.Br. extract on ethanol-mediated oxidative damage in rat kidney

Abstract

The antioxidant effect of the ethanolic extract of Hemidesmus indicus R.Br. root (EHI), an indigenous Ayurvedic medicinal plant in India, was studied in rats with ethanol-induced nephrotoxicity. Administering 5 g/kg body weight/day of ethanol for 60 days to male Wistar rats resulted in significantly elevated levels of serum urea, creatinine and uric acid as well as kidney thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH) and conjugated dienes (CD) as compared to those of the experimental control rats. Decreased levels of kidney superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), vitamin C and vitamin E were also observed on alcohol administration as compared with those of the experimental control rats. EHI was administered at a dose of 500 mg/kg body weight/day for the last 30 days of the experiment to rats with ethanol-induced kidney injury, which significantly decreased the levels of serum urea, uric acid and creatinine as well as kidney TBARS, LOOH and CD and significantly elevated the activities of SOD, CAT, GPx, GSH, vitamin C and vitamin E in kidney as compared to that of untreated ethanol-administered rats. Histopathological observations also correlated with the biochemical parameters. Thus, the data indicate that treatment with EHI offers protection against free radical-mediated oxidative stress in kidney of animals with ethanol-induced nephtrotoxicity.     

Comparative study of oxidative stress and antioxidative markers in patients infected with Toxoplasma gondii

Recently, oxidative stress and antioxidative compounds have been described as potential biomarkers. However, there is no consensus on the most appropriate oxidative and antioxidative biomarkers for patients with Toxoplasma gondii. In the present study, we evaluated the levels of lipid, protein, DNA oxidative damage and antioxidants in samples from patients infected with T. gondii with and without ocular toxoplasmosis. The levels of MDA, TBARS, micronuclei, carbonyl, GSH, vitamin C and vitamin E were measured on samples from 8 patients positive for T. gondii antibodies with ocular toxoplasmosis (OT), 20 patients positive for T. gondii antibodies without ocular toxoplasmosis (non OT), and 12 healthy individuals negative for T. gondii antibodies. The levels of MDA, TBARS, carbonyl and micronuclei were significantly higher in non OT patients, while MDA and TBARS levels were lower in OT patients. In contrast, the antioxidative factors, GSH and vitamin E levels were significantly lower in non OT patients, while vitamin C was lower in non OT and OT patients. Additionally, non OT patients were indicated to be high producers of oxidative markers (TBARS, MDA, micronuclei and carbonyl), while control group was indicated to be high producer of antioxidative markers (GSH, vitamins C and E). However, OT patients were not found as high producers of oxidative nor antioxidative markers. Our results provide a starting point of possible markers to better understand the disease pathogenesis in patients infected with T. gondii. Additional studies are needed to clarify the potential contribution of oxidative and antioxidative markers in these patients population.     

Effects of temperature on modulation of oxidative stress and antioxidant defenses in testes of tropical tasar silkworm Antheraea mylitta

High temperatures are known to cause physiological stress in organisms. This is often associated with enhanced generation of reactive oxygen species (ROS) leading to oxidative damage. The commercially important tropical tasar silkworm Antheraea mylitta has to endure high summer temperature before egg production on the onset of monsoon. In this study the status of pro-oxidants and antioxidants was studied in the testes of male pupae of tasar silkworm A. mylitta under thermal stress condition. Further, to find out the impact of temperature on physiological activity, oxygen consumption rate was measured. The result indicated higher level of thiobarbituric acid reactive substances (TBARS, as an index of lipid peroxidation) and total hydroperoxides in the male pupae exposed to high temperature (40±1 °C). Similarly, it was found that increased levels of antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), ascorbic acid (ASA) and low molecular thiols (L-SH) in testes are more prominent in high temperature rather than in moderate temperature (35±1 ^oC) suggesting the activation of physiological mechanism to scavenge the ROS produced during stress. Further more, the order of higher level of oxygen consumption rate was observed as high temperature (40±1°C) > moderate temperature (35±1°C) > control groups (28±1°C). Oxygen consumption rate was positively correlated with oxidative stress and antioxidant defence indices. We infer from these findings that the testes of A. mylitta pupae modulate testicular antioxidant responses to thermal stress.     

Activity of Cassia auriculata leaf extract in rats with alcoholic liver injury

This study was undertaken to investigate the effect of Cassia auriculata leaf extract on tissue lipid peroxidation and antioxidant status in experimental hepatotoxicity. Administering ethanol to rats for 60 days resulted in significantly elevated levels of serum total bilirubin, aspartate transaminase (AST), alanine transaminase (ALT) and alkaline phosphatase (ALP) as compared with those of the experimental control rats. Significantly elevated levels of tissue thiobarbituric acid reactive substances (TBARS), hydroperoxides and lowered activities of superoxide dismutase (SOD), catalase (CAT) and reduced glutathione (GSH) were also observed on alcohol treatment as compared with those of experimental control rats. Concentration of serum non-enzymic antioxidants such as vitamin E and vitamin C were also significantly lowered on alcohol supplementation. Treatment with Cassia auriculata leaf extract at a dose of 250 mg kg(-1) body weight and 500 mg kg(-1) body weight to rats administered alcohol, lowered the levels of TBARS and hydroperoxides and elevated the activities of SOD and CAT and the levels of reduced GSH in the liver, brain, kidney and intestine significantly compared to unsupplemented alcohol treated rats. Cassia auriculata leaf extract treatment restored the serum vitamin E, and vitamin C levels also to near those of the experimental control animals. Our data indicate that supplementation with Cassia auriculata leaf extract can offer protection against free radical mediated oxidative stress in experimental hepatotoxicity. In addition, histopathological studies of the liver and brain confirmed the beneficial role of Cassia auriculata leaf extract.     

Evaluation of oxidative damage in the liver of selenium-deficient rats

Previous studies have implied a relationship between Se-deficiency and oxidative stress. In the present study, the occurrence of oxidative stress due to Se-deficiency was investigated by evaluating the age dependence of growth and indices of oxidative damage for the liver of Se-deficient (SeD) rats. The ratios of liver weight to body weight of the SeD rats were greater than those of the normal rats. The values of AST and ALT (clinical indices of liver damage) were higher in the SeD rats than the normal ones especially in the young (6-12 weeks of age). The TBARS level of the 4-week-old SeD group were higher than the normal group while the level decreased with age. Conversely, the TBARS level of the normal group gradually increased and became higher than SeD group in older rats (12-20 weeks of age). Vitamin E rather than vitamin C may be consumed during oxidative stress due to Se-deficiency. Damage induced by Se-deficiency may be related to growth and the mechanisms of this damage may alter with age.     

QUERCETIN EFFECTS ON WEIGHT GAIN AND CALORIC INTAKE IN EXERCISED RATS

Quercetin is a flavonoid which activates oxidative metabolism. Quercetin may reduce weight gain by decreasing feed efficiency. The present study aims to evaluate weight gain, caloric intake and feed efficiency in exercised and sedentary rats supplemented with quercetin. Wistar rats were divided into four groups: quercetin-exercise training (QT), quercetin-sedentary (QS), placebo-exercise training (PT) and placebo-sedentary (PS). Rats were exercised and/or orally supplemented with quercetin (25 mg · kg⁻¹ on alternate days) during six weeks. Weight gain of the QT group decreased when compared with the PT and PS groups. Exercised groups increased cumulative caloric intake during the experimental period. The QT group rats also reduced their feed efficiency when compared with the QS and PS groups. These results suggest that quercetin is not able to decrease weight gain because no differences were found between placebo and quercetin condition either in the sedentary or in the training condition.     

Effects of aging on the susceptibility to the toxic effects of cyclosporin A in rats. Changes in liver glutathione and antioxidant enzymes

Free radicals are involved in aging and cyclosporin A-induced toxicity. The age-related changes in the liver oxidative status of glutathione, lipid peroxidation, and the activity of the enzymatic antioxidant defense system, as well as the influence of aging on the susceptibility to the hepatotoxic effects of cyclosporin (CyA) were investigated in rats of different ages (1, 2, 4, and 24 months). The hepatic content of reduced glutathione (GSH) increased with aging, peaked at 4 months, and decreased in senescent rats. By contrast, glutathione disulfide (GSSG) and thiobarbituric acid-reactive substances (TBARS) concentrations and superoxide dismutase, catalase, and glutathione peroxidase activities were higher in the oldest than in the youngest rats. CyA treatment, besides inducing the well-known cholestatic syndrome, increased liver GSSG and TBARS contents and the GSSG/GSH molar ratio, and altered the nonenzymatic and enzymatic antioxidant defense systems. The CyA-induced cholestasis and hepatic depletion of GSH, and the increases in the GSSG/GSH ratio, and in GSSG and TBARS concentrations were higher in the older than the mature rats. Moreover, superoxide dismutase and catalase activities were found to be significantly decreased only in treated senescent rats. The higher CyA-induced oxidative stress, lipoperoxidation, and decreases in the antioxidant defense systems in the aged animals render them more susceptible to the hepatotoxic effects of cyclosporin.     

Oxidative damage of rat cerebral cortex and hippocampus,and changes in antioxidative defense systems caused by hyperoxia

In order to elucidate the oxidative damage in rat brain caused by oxidative stress, regional changes in the levels of lipid peroxidation products and antioxidative defense systems in cerebral cortex and hippocampus, and in their synapses, which modulate learning and memory functions in the brain, were studied. When rats were subjected to hyperoxia as an oxidative stress, thiobarbituric acid reactive substance (TBARS) in the regions studied increased more than in normal rats by approximately 35%. The values in oxygen-unexposed vitamin E-deficient rats were also higher than in normal rats. It was found that the TBARS contents in synaptosomes isolated from both regions were remarkably higher than in the organs. These results imply that synapses are more susceptible to oxidative stress than the organ itself. This tendency was also observed in the content of conjugated diene. In response to oxidative stress, the status of the antioxidant defense system in each region, i.e. the concentration of vitamin E, and the activities of superoxide dismutase, catalase and glutathione peroxidase, decreased remarkably. On the other hand, in oxygen-unexposed vitamin E-deficient rats, the activities of these enzymes in each region tended to increase, except for catalase activity. These results suggest that in response to the oxidative stress, the antioxidant defense systems may be consumed to prevent oxidative damage, and then, may be supplied through the antioxidant network.     

Effect of stress-induced lipid peroxidation on functions of rat peritoneal macrophages

The aim of the present study was to investigate the effects of stress-induced lipid peroxidation on macrophages' functions. Animals were subjected to 4 h immobilization at 4 degrees C in restraining devices. The peritoneal macrophages obtained from rats exposed to cold and restraint stress exhibited an increase in lipid peroxidation and a decline of chemotaxis and phagocytosis compared with control rats. After supplementation with vitamin E, the increment in thiobarbituric acid reactive substances (TBARS) content as the oxidative stress marker and the decline of chemotaxis and phagocytosis in peritoneal macrophages observed during cold-restraint stress was significantly removed. No significant change in catalase activity of peritoneal macrophages was observed in groups exposed to cold-restraint stress and treated with vitamin E. These findings indicate that phagocytic and chemotactic capacities of peritoneal macrophages are decreased by cold-restraint stress and this effect of stress may be related to lipid peroxidation.     

Efficacy of some antioxidants supplementation in reducing oxidative stress post sodium tungstate exposure in male wistar rats

This study aimed to evaluate the protective efficacy of some antioxidants against sodium tungstate induced oxidative stress in male wistar rats. Animals were sub-chronically exposed to sodium tungstate (100 ppm in drinking water) for three months except for control group. In the same time, many rats were supplemented orally with different antioxidants (alpha-lipoic acid (ALA), n-acetylcysteine (NAC), quercetin or naringenin (0.30 mM)) for five consecutive days a week for the same mentioned period before. Exposure to sodium tungstate significantly (P < 0.05) inhibit blood δ-aminolevulinic acid dehydratase (ALAD) activity, liver and blood reduced glutathione (GSH) levels and an increase in oxidized glutathione (GSSG) and thiobarbituric acid reactive species (TBARS) levels in tissues. ALA acid and NAC supplementation post sodium tungstate exposure increased GSH and also, was beneficial in the recovery of altered superoxide dismutase and catalase activity, besides, significantly reducing blood and tissue reactive oxygen species and TBARS levels. The results suggest a more pronounced efficacy of ALA acid and NAC supplementation than quercetin or naringenin supplementation post sodium tungstate exposure in preventing induced oxidative stress in rats.     

茄子光系统Ⅱ的热胁迫特性

以耐热性较弱的黑贝一号圆茄和耐热性较强的黑贝二号圆茄为试材,热胁迫处理后采用植物效率仪PEA进行快速叶绿素荧光诱导曲线及其参数测定.结果表明：当温度高于40 ℃,PSⅡ结构受热胁迫影响较为敏感,表现为初始荧光F_o缓慢上升;PSⅡ原初光化学效率F_v/F_m和ΔF/F_m′大幅度下降,且黑贝二号F_v/F_m的半衰时间T₅₀和ΔF/F_m′的半衰温度t₅₀分别大于黑贝一号.较高的热胁迫剂量（48℃处理5 min或44℃处理20～30min）下,快速荧光诱导动力学曲线呈现OKJIP型,在700μs处出现与放氧复合体失活有关的K相.黑贝一号在44 ℃下处理20 min才有K相出现,黑贝二号则晚10 min出现.与35℃相比,在48℃,特别是在52℃的较高剂量热胁迫下,Strasser能量流动模型参数中的DI_o/RC有大幅度地增加,体现了热耗散对PSⅡ的较强保护能力.随着热胁迫温度的升高和热胁迫时间的延长,两品种的无活性中心F_vi/Fv显著增加.     

Influences of different stress models on the antioxidant status and lipid peroxidation in rat erythrocytes

The aim of this study was to investigate the influences of different stress models on the antioxidant status and lipid peroxidation (LPO) in erythrocytes of rats. Swiss-Albino female rats (3 months old) were used in this study. Rats were randomly divided into the following four groups; control group (C), cold stress group (CS), immobilization stress group (IS) and cold+immobilization stress group (CS+IS). Control group was kept in an animal laboratory (22 ±2°C). Rats in CS group were placed in cold room (5°C) for 15 min/day for 15 days. Rats in IS group were immobilized for 180 min/day for 15 days. Rats in CS+IS group were exposed to both cold and immobilization stresses for 15 days. At the end of experimental periods, the activities of glucose-6-phosphate dehydrogenase (G-6-PD), Cu,Zn-superoxide dismutase (Cu,Zn-SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), and concentration of reduced glutathione (GSH) were measured. LPO was determined by measuring the contents of thiobarbituric acid-reactive substances (TBARS). Cu,Zn-SOD activity and TBARS concentration were increased after cold and immobilization stresses, but CAT and GSH-Px activities and GSH levels were decreased. Immobilization stress decreased the activity of G-6-PD. The activities of G-6-PD, CAT and GSH-Px, and the level of GSH were lower in CS+IS group than in the control group. Cu,Zn-SOD activity and TBARS levels were increased in CS+IS group when compared with the control group. From these findings, three stress models are thought to cause oxidative stress.     

Influences of Different Stress Models on the Antioxidant Status and Lipid Peroxidation in Rat Erythrocytes

The aim of this study was to investigate the influences of different stress models on the antioxidant status and lipid peroxidation (LPO) in erythrocytes of rats. Swiss-Albino female rats (3 months old) were used in this study. Rats were randomly divided into the following four groups; control group (C), cold stress group (CS), immobilization stress group (IS) and cold+immobilization stress group (CS+IS). Control group was kept in an animal laboratory (22 &#45 2°C). Rats in CS group were placed in cold room (5°C) for 15 min/day for 15 days. Rats in IS group were immobilized for 180 min/day for 15 days. Rats in CS+IS group were exposed to both cold and immobilization stresses for 15 days. At the end of experimental periods, the activities of glucose-6-phosphate dehydrogenase (G-6-PD), Cu,Zn-superoxide dismutase (Cu,Zn-SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), and concentration of reduced glutathione (GSH) were measured. LPO was determined by measuring the contents of thiobarbituric acid-reactive substances (TBARS). Cu,Zn-SOD activity and TBARS concentration were increased after cold and immobilization stresses, but CAT and GSH-Px activities and GSH levels were decreased. Immobilization stress decreased the activity of G-6-PD. The activities of G-6-PD, CAT and GSH-Px, and the level of GSH were lower in CS+IS group than in the control group. Cu,Zn-SOD activity and TBARS levels were increased in CS+IS group when compared with the control group. From these findings, three stress models are thought to cause oxidative stress.     

Effects of angiotensin II type 1 receptor blockade on the oxidative stress in spontaneously hypertensive rat tissues

The aim of this work was to investigate the production of oxidative damage in homogenized kidney, liver and brain of spontaneously hypertensive rats (SHR), as well as the involvement of angiotensin (Ang) II in this process. Groups of 12-week-old SHR and Wistar Kyoto rats (WKY) were given 10 mg/kg/day losartan in the drinking water during 14 days. Other groups of WKY and SHR without treatment were used as controls. The production of thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH) and the activity of the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (Gpx) were determined. No significant difference in TBARS was observed between untreated SHR or WKY rats; GSH content was lower in the liver but higher in the brain of SHR compared to WKY rats. In tissues from the SHR group, SOD and Gpx activities were reduced, whereas CAT activity was slightly increased in kidney. TBARS levels did not change in WKY rats after losartan administration, but were reduced in SHR liver and brain. Losartan treatment decreased GSH content in WKY kidney, but increased GSH in SHR liver. The activity of the antioxidant enzymes was not modified by losartan in WKY rats; however, their activities increased in tissues from treated SHR. The lower activity of antioxidant enzymes in tissues from hypertensive rats compared to those detected in normotensive controls, indicates oxidative stress production. Ang II seems to play no role in this process in normotensive animals, although AT1 receptor blockade in SHR enhances the enzymatic activity indicating that Ang II is implicated in oxidative stress generation in the hypertensive animals.