Male Wistar Strain Rats Research Articles

Age-related oxidative protein damages in central nervous system of rats: modulatory role of grape seed extract

Oxidative stress has been shown to play a major role in aging and in neurodegenerative disorders. Protein modification is one of the important consequences of oxidative stress. In the present study, we evaluated the role of grape seed extract on memory, reactive oxygen species production, protein carbonyls (PCO), and thiol status in discrete regions of central nervous system of young and aged rats. Male albino rats of Wistar strain were divided into four groups: Group I—control young rats, Group II—young rats treated with grape seed extract (100mg/kg BW) for 30 days, Group III—aged control rats and Group IV—aged rats supplemented with grape seed extract (100mg/kg BW) for 30 days. Memory loss was observed in the aged rats. Age associated increase in reactive oxygen species production and protein oxidation was observed in the spinal cord; cerebral cortex, striatum and the hippocampus regions of aged rats (Group III). The levels of total thiol, non-protein thiol, protein thiols were found to be significantly decreased in spinal cord and all the brain regions studied in aged rats when compared to young rats. Supplementation of aged rats with grape seed extract showed increased memory performance and declined reactive oxygen species production, decreased protein carbonyl levels and improved thiol levels. These findings demonstrated that grape seed extract enhanced the antioxidant status and decreased the incidence of free radical induced protein oxidation in aged rats thereby protecting the central nervous system from the reactive oxygen species.

Characteristics of rat round spermatids differentiated from spermatogonial cells during co-culture with Sertoli cells, assessed by flow cytometry, microinsemination and RT-PCR

The present study was undertaken to investigate whether rat spermatogonial stem cells can differentiate into developmentally competent round spermatids during co-culture with Sertoli cells. Type-A spermatogonia and Sertoli cells were prepared from 7-d-old Wistar-strain male rats, and seeded at 4 × 10 6 cells/4 mL/35-mm dish (Day 0). They were co-cultured at 37 °C for 3 d and at 34 °C for the subsequent 7 d in 5% CO 2/air. Round spermatid-like cells (approximately 15 μm in diameter) were first observed on Day 5. A flow cytometric analysis showed that a single peak of haploid cells was detected in the cell populations harvested on Day 10. The participation of the spermatid-like cells to full-term development was examined by microinjection into activated oocytes. The oviductal transfer of 143 microinseminated oocytes resulted in only 8 implantation sites (6%), but no viable offspring. The expression of the round spermatid-specific marker gene, PRM-2, was confirmed in the Day 10 cell population by RT-PCR; however, no mRNA of two other haploid makers, TP1 or TP2, was detected. These results suggested that rat type-A spermatogonial cells underwent meiosis during the primary co-culture with the Sertoli cells, based on morphology, flow cytometry and PRM-2 expression, but the normality of the spermatid-like cells was not supported by microinsemination and TP1/2 expression.

Protective effect of lipoic acid on adriamycin-induced testicular toxicity

Background Adriamycin (ADR), an anthracycline antibiotic, which is widely used as an antineoplastic drug in the treatment of various solid tumors, has been shown to induce reproductive abnormalities in males. In the present study, the effect of lipoic acid (LA), a universal antioxidant, was investigated on ADR-induced testicular toxicity in rats. Methods Adult male albino rats of Wistar strain were administered ADR (1 mg/kg body weight, i.v.), once a week for 10 weeks. Semen quality was evaluated in terms of sperm count, percentage motility and abnormality. The testicular damage was also assessed by the measurement of marker enzymes activities and histology. Results ADR treated rats showed a significant decrease in sperm count and motility while an increase in dead and abnormal sperms. The activities of testicular marker enzymes such as γ-glutamyl transferase, β-glucuronidase, acid phosphatase and alkaline phosphatase were increased whereas the activity of lactate dehydrogenase-X was decreased significantly in the animals treated with ADR. ADR treated rats also showed abnormal histologic findings. Treatment with lipoic acid (35 mg/kg body weight, i.p.) 1 day prior to ADR administration, improved the semen quality and maintained near normal activities of the enzymes. Conclusion By the reversal of biochemical and morphological changes towards normalcy, the cytoprotective role of LA is illuminated in ADR-induced testicular toxicity.

Cardioprotective effect of pentacyclic triterpene, lupeol and its ester on cyclophosphamide-induced oxidative stress

Cyclophosphamide (CP), an alkylating agent widely used in cancer chemotherapy, causes fatal cardiotoxicity. In the present study, lupeol, a pentacyclic triterpene, isolated from Crataeva nurvala stem bark and its ester, lupeol linoleate were investigated for their possible cardioprotective effects against CP-induced toxicity. Male albino rats of Wistar strain were injected with a single dose of CP (200 mg/kg body weight, ip). In CP-administered rats, activities of lactate dehydrogenase and creatine phosphokinase were elevated in serum with a concomitant decline in their activities in the cardiac tissue. Significant increases (P<0.001) in the levels of lipid peroxides and a decrease (P<0.001) in the levels of enzymic (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase and glutathione-s-transferase) and nonenzymic (reduced glutathione, vitamin C and vitamin E) antioxidants in the heart were also observed. The cardioprotective effects of lupeol (50 mg/kg body weight for 10 days orally) and its ester, lupeol linoleate (50 mg/kg body weight for 10 days orally) were evident from the significant reversal of the above alterations induced by CP. These observations highlight the antioxidant property of triterpenes and their cytoprotective action against CP-induced cardiotoxicity.

Rejuvenation of antioxidant system in central nervous system of aged rats by grape seed extract

Oxidative stress is considered as a major risk factor that contributes to age-related increase in lipid peroxidation and declined antioxidants in the central nervous system during aging. Grape seed extract, one of the bioflavonoid, is widely used for its medicinal properties. In the present study, we evaluated the role of grape seed extract on lipid peroxidation and antioxidant status in discrete regions of the central nervous system of young and aged rats. Male albino rats of Wistar strain were divided into four groups: Group I—control young rats, Group II—young rats treated with grape seed extract (100 mg/kg body weight) for 30 days, Group III—aged control rats and Group IV—aged rats supplemented with grape seed extract (100 mg/kg body weight) for 30 days. Age-associated increase in lipid peroxidation was observed in the spinal cord, cerebral cortex, striatum and the hippocampus regions of aged rats (Group III). Activities of antioxidant enzymes like superoxide dismutase, catalase, glutathione peroxidase and levels of non-enzymic antioxidants like reduced glutathione, Vitamin C and Vitamin E were found to be significantly decreased in all the brain regions studied in aged rats when compared to young rats. However, normalized lipid peroxidation and antioxidant defenses were reported in the grape seed extract-supplemented aged rats. These findings demonstrated that grape seed extract enhanced the antioxidant status and decreased the incidence of free radical-induced lipid peroxidation in the central nervous system of aged rats.

Possible role of calcineurin in heating-related increase of rat muscle mass

The purpose of this study was to investigate the contribution of calcineurin-related intracellular signal for heat-stress-associated muscle hypertrophy. Wistar strain male rats (7-week-old) were randomly divided into four groups: (1) control (CC, n = 15), (2) control with the injection of cyclosporine A (CsA) (CA, n = 15), (3) heat-stressed (HC, n = 15), and (4) heat-stressed with the injection of CsA (HA, n = 15). The heat-stress groups (HC and HA) were exposed to heat (41 °C for 60 min) in a controlled heat chamber without anesthesia. Soleus and extensor digitorum longus (EDL) muscles were dissected and weighed 1, 7, and 14 days after the exposure. Wet and dry weights of soleus were increased 7 days following heat exposure. The expressions of heat shock protein 72 (HSP72) and calcineurin in both muscles were also increased within 1 and 7 days following heat-stress, respectively. Administration of CsA, a specific inhibitor for calcineurin, depressed heat-stress-associated increase of muscle weight and calcineurin expression, especially in soleus. These observations suggest that a calcineurin-dependent signaling pathway may play an important role in the heat-stress-related skeletal muscular hypertrophy. Application of heat-stress to skeletal muscles may be a useful tool to gain muscular mass and force generation not only in athletes, but also in patients during rehabilitation.

Effects of chronic ingestion of sodium fluoride on myocardium in a second generation of rats

Possible effects of long term exposure (6 months) to sodium fluoride (NaF) through drinking water on the morphology and biochemistry of myocardial tissue in second generation adult male rats were investigated. Wistar strain female and male rats were reared until the second generation of rats obtained, during which they were given 1, 10, 50 and 100 mg/L NaF in drinking water. Of the second generation, 28 male rats were divided into four groups and had the same treatment. All the second generation rats were sacrificed and autopsied at the end of the 6 months. In the samples of myocardial tissues, the levels of serum fluoride and the activities of principal antioxidant enzymes were determined, and a histopathological examination was conducted. Significant histopathological changes were found in the myocardial tissue of rats treated with 50 and 100 mg/L NaF. These were myocardial cell necrosis, extensive cytoplasmic vacuole formation, nucleus dissolution in myosits, swollen and clumped myocardial fibers, fibrillolysis, interstitial oedema, small hemorrhagic areas and hyperaemic vessels. Additionally, the increased activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and thiobarbituric acid-reactive substance (TBARS) levels were observed in the myocardial tissues of rats treated with 10 and 50 mg/L NaF. On the other hand, the activities of SOD, GSH-Px, and CAT decreased, but the TBARS levels increased in the myocardial tissues of rats treated with 100 mg/L. The present results revealed that prolonged ingestion of fluoride through drinking water, particularly with high doses, induced significant histopathological and biochemical changes leading to myocardial tissue damage.

Lipoic acid ameliorates adriamycin-induced testicular mitochondriopathy

Adriamycin (ADR), an anthracycline antibiotic, which is widely used as an antineoplastic drug in the treatment of various solid tumors, has been shown to induce reproductive abnormalities in males. In the present study, the effect of lipoic acid (LA), a universal antioxidant was investigated on ADR-induced testicular toxicity in rats. Adult male albino rats of Wistar strain were administered ADR (1 mg/kg body weight, i.v.), once a week for 10 weeks. Mitochondrial fractions of the testis were obtained by differential centrifugation. The activities of mitochondrial antioxidant enzymes such as superoxide dismutase, glutathione peroxidase and glutathione reductase were decreased significantly in the animals treated with ADR. The levels of mitochondrial lipid peroxides and hydrogen peroxide were increased in ADR-treated rats. ADR-treated rats also showed decline in the activities of mitochondrial enzymes such as succinate dehydrogenase (SDH), malate dehydrogenase (MDH) and isocitrate dehydrogenase (ICDH). Treatment with lipoic acid (35 mg/kg body weight, i.p.) 1 day prior to ADR administration, maintained near normal activities of the enzymes, thereby proving to be an effective cytoprotectant.

Ascorbic acid and α-tocopherol as potent modulators of apoptosis on arsenic induced toxicity in rats

Apoptosis or programmed cell death (PCD) is a genetically regulated cellular, physiological and biochemical suicidal mechanism that plays a crucial role in the development and defense of homeostasis, in which the cell participates in its own demise via a cascade of molecular interactions. PCD can be modulated by various stimuli including infectious agents or drugs. Arsenic is one among inducible toxic agent that triggers apoptosis via free radical generation. Since the generation of free radicals during the metabolism of arsenic is thought to be involved in arsenic toxicosis, understanding the deleterious effects caused by the ROS that attack the vital molecules like DNA has become important. The present work was conducted to evaluate the regulatory effect exerted by Vitamin C and Vitamin E upon the apoptotic process, which can be assessed by the presence of cells with apoptosis associated DNA breaks and characterize the role of TNF-α and caspase-3 in rats intoxicated with arsenic. Male albino rats of wistar strain (120–150 g) were used in this study and are further divided into seven groups. We observed that ascorbate and α-tocopherol selectively altered the extent of DNA damage by reducing TNF-α level and inhibiting the activation of caspase cascade, from these observations it is strongly believed that the present vitamins supplementation perspective, though observed in animal model, will have sustainable curative value among the already afflicted populations, neutralizing impact on freshly emerging arsenicosis scenario and possible proactive protection to those potentially susceptible to arsenicals exposure.

ラット下顎切歯抜歯窩の治癒過程に関する研究

Prosthodontic treatment is difficult if the alveolar ridge is low or thin. To develop a method for alveolar ridge preservation after tooth extraction, we need an experimental model of a small animal, in which we can analyze the socket healing easily and quantitatively. The purpose of the present study was to establish such an experimental model. Ten weeks old male rats of Wistar strain were used. The edge of the right mandibular incisor was cut every three days three times and the incisor was extracted at three days after the final cut. The animals were sacrificed 0, 1, 2, 4, 8, 12 weeks after the extraction and the mandibles were dissected out. The length of the alveolar bone was measured on soft X-ray photographs and bone mineral content was measured with a dual energy X-ray absorptiometer (DEXA). Then, transverse sections of the alveolar bone were prepared. Periodic three-times cutting of the edge of the mandibular incisor made the extraction easy. Quantitative analyses of new bone formation in the socket and the resorption of the alveolar bone were possible with soft X-ray photography and DEXA. The histological findings corresponded well with the data from the soft X-ray photos and DEXA measurements. The present results demonstrated the possibility of simple and quantitative analyses of socket healing after the extraction of rat mandibular incisors. This experimental model would be useful for developing a method to prevent atrophy of the alveolar ridge after tooth extraction.

Effect of Chitin-Chitosan Treatment on Fatty Liver in Rats with a High Fat Diet

The present study was designed to investigate the hepatoprotective effect of 2% chitin-chitosan mixture on high fat diet-induced fatty liver, an experimental model for non-alcoholic fatty liver disease, in Wistar strain male rats. The hepatoprotective property was determined based on the following criteria: total lipid in liver, concentrations of total cholesterol, triglycerides, free fatty acids and phospholipids of serum and liver tissue; liver lipid/protein ratio; serum and tissue activities of aspartate amino transferase (AST) and alanine amino transferase (ALT); fecal fat determination and activity of pancreatic lipase. Chitin-chitosan fed animals gained less weight compared to the controls. A significant (p < 0.001) reduction in the liver lipid/protein ratio was observed in chitin-chitosan mixture supplemented rats as compared to that of control animals. Also the blood and liver fat, cholesterol, triglycerides, free fatty acids and phospholipid concentrations, decreased significantly by chitin-chitosan supplementation. Serum levels of aspartate aminotransferase and alanine aminotransferase showed significant (p < 0.001) reduction while tissue levels exhibited a concomitant increase upon chitin-chitosan treatment. Enhanced fat excretion (p < 0.001) was observed in the chitin-chitosan supplemented group. In the present study, supplementation of chitin-chitosan mixture did not induce any significant change in the activity of pancreatic lipase as compared to normal animals. This indicates that the antilipidaemic effect of chitin-chitosan mixture supplementation was mainly due to the interference in the gastrointestinal absorption of dietary fat rather than the mixture having any direct role on lipid metabolism. In conclusion, dietary supplementation of chitin-chitosan mixture can alleviate the high fat diet-induced aberrations related to lipid metabolism in fatty liver of experimental animals by their antilipidaemic property.

Protective Role of a Novel Curcuminoid on Alcohol and PUFA-Induced Hyperlipidemia

Alcohol use is contributing to an unprecedented decline in life expectancy. It induces hyperlipidemia when taken at higher concentrations. Alcoholics usually after a heavy binge of alcohols take fried food items normally made up of polyunsaturated fatty acids (PUFAs). The combined ingestion of alcohol and PUFAs is considered to be dangerous and known to result in hyperlipidemic conditions. Previous studies have shown that curcumin, an active principle of turmeric (Curcuma longa), has antihyperlipidemic properties. So in the present work we have synthesized an analog of curcumin and tested the protective role of that synthetic curcuminoid on alcohol and thermally oxidized sunflower oil-induced hyperlipidemia. Male Albino rats of Wistar strain were used for the experimental study. Antihyperlipidemic activity of the synthetic curcuminoid was evaluated by analyzing the levels of lipids (cholesterol, triglycerides [TGs], phospholipids [PLs], and free fatty acids [FFAs]) in different tissues and histopathological changes in the liver. The results showed that the levels of cholesterol, TGs, and FFAs were increased significantly in alcohol, thermally oxidized sunflower oil (Δ PUFA), and alcohol + Δ PUFAs treated groups. Administration of synthetic curcuminoid effectively reduced these levels. The phospholipid (PL) levels, which were decreased in the liver and kidney and increased in the heart in the alcohol, Δ PUFA, and alcohol + Δ PUFA groups, were positively modulated by treatment with synthetic curcuminoid (CA). Our histopathological observations were also in correlation with the biochemical parameters. From the results obtained, we could conclude that the synthetic curcuminoid effectively protects the system against alcohol and Δ PUFA-induced hyperlipidemia and may become an effective therapeutic agent for the treatment of hyperlipidemia.

Counteracting adriamycin-induced oxidative stress by administration of N-acetyl cysteine and vitamin E

Adriamycin (ADR), a cytotoxic antineoplastic drug, is used in the treatment of various solid tumors. However, its efficacy continues to be challenged by significant toxicities including nephrotoxicity. In the present study, the effects of N-acetyl cysteine (NAC) and vitamin E, known antioxidants, were investigated on ADR-induced peroxidative damage in rat kidney. Adult male albino rats of Wistar strain were administered ADR as a single dose (10 mg/kg body weight, i.v.). Histopathological studies indicated that ADR-treated kidney sections show focal tubular necrosis and casts. ADR-injected rats showed a significant decline in the activities/levels of enzymic antioxidants (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase and glutathione-S-transferase) and non-enzymic antioxidants (thiols, vitamin C and vitamin E) with high malondialdehyde levels. The extent of nephrotoxicity was evident from the increased activities of urinary marker enzymes (alkaline phosphatase, lactate dehydrogenase and gamma-glutamyltransferase). Treatment with NAC and vitamin E (50 mg/kg b.w., i.p.) 1 day prior to ADR administration maintained near normal activities of the enzymes, significantly reduced lipid peroxidation and prevented the necrosis caused by ADR, thereby proving to be an effective thiol replenishing agent and antioxidant.

Remedial effect of DL- -lipoic acid against adriamycin induced testicular lipid peroxidation

Adriamycin (ADR), a cytotoxic antineoplastic drug is used in the treatment of various solid tumors. However, its efficacy continues to be challenged by significant toxicities including testicular toxicity. In the present study, the effect of lipoic acid, a "universal antioxidant" was investigated on ADR induced peroxidative damages in rat testis. Adult male albino rats of Wistar strain were administered ADR (1 mg/kg body weight, i.v.) once a week for 10 weeks. ADR injected rats showed a significant decline in the activities of enzymic antioxidants (catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase) and non-enzymic antioxidants (reduced glutathione, Vitamin A, Vitamin C and Vitamin E) with high malondialdehyde levels. The extent of testicular toxicity was evident from the decreased activities of testicular marker enzymes (sorbitol dehydrogenase and glucose-6-phosphate dehydrogenase). Treatment with lipoic acid (35 mg/kg body weight, i.p.) one day prior to ADR administration, maintained near normal activities of the enzymes and significantly reduced lipid peroxidation, thereby proving it to be an effective cytoprotectant.

Species difference in cholesterol 7α-hydroxylase expression of rabbit and rat liver microsomes after bile duct ligation

Background Bile duct ligation (BDL) produces a good animal model for investigation of the metabolic changes in obstructive jaundice. The aim of this study was to investigate the species difference in expression of cholesterol 7α-hydroxylase (7α-hydroxylase) in rabbits and rats after BDL. Materials and methods Ten male New Zealand white rabbits weighing 2.5–3 kg and 12 male Wistar strain rats weighing 250–300 g were used. Half the animals underwent BDL, and half were sham operated (Sham). The animals were sacrificed on day 5 after operation. The livers were harvested, and levels of mRNA and 7α-hydroxylase activity were determined. Concentrations of serum bilirubin and bile acids were also measured. Results In BDL rats, the levels of mRNA were increased 30%, and 7α-hydroxylase activity was three times that of the Sham group. In BDL rabbits, however, these values were approximately 60 and 50% lower than the Sham group, respectively. Serum bile acid concentrations increased up to 13 times in BDL rabbits and 70 times in BDL rats over that of the Sham groups. Serum cholesterol and serum total bilirubin concentration also increased after BDL in both animals. Conclusion These results suggest that there is a species difference in the expression of 7α-hydroxylase after BDL in rabbits and rats and the reason for this difference is most likely pretranslational regulation.

Polymorphism in Diazepam Metabolism in Wistar Rats

We observed variations in the metabolism of diazepam in Wistar rats. We studied these variations carefully, and found that the variations are dimorphic and about 17% of male rats of Wistar strain we examined showed two times higher diazepam metabolic activities in their liver microsomes than the rest of animals at the substrate concentrations less than 5 μM. We classified them as extensive metabolizer (EM) and poor metabolizer (PM) of diazepam. No sex difference was observed in the frequency of appearance of EM. Activities of the primary metabolic pathways of diazepam were examined to elucidate the cause of this polymorphism in male Wistar rats. No significant differences were observed in activities of neither diazepam 3-hydroxylation or N-desmethylation between EM and PM rats, while activity of diazepam p-hydroxylation was markedly (more than 200 times) higher in EM rats, indicating that this reaction is responsible for the polymorphism of diazepam metabolism in Wistar rats. We examined the expression levels of CYP2D1, which was reported to catalyze diazepam p-hydroxylation in Wistar rats to find no differences in the expression levels of CYP2D1 between EM and PM rats. The kinetic study on diazepam metabolism in male Wistar rats revealed that EM rats had markedly higher Vmax and smaller Km in diazepam p-hydroxylation than those of PM rats, indicating the presence of high affinity high capacity p-hydroxylase enzyme in EM rats. As a consequence, at low concentrations of diazepam, major pathways of diazepam metabolism were p-hydroxylation and 3-hydroxylation in male EM rats, while in male PM rats, 3-hydroxylation followed by N-desmethylation. Due to this kinetic nature of p-hydroxylase activity, EM rats had markedly higher total CLint of diazepam than that of PM rats. Polymorphism in diazepam metabolism in humans is well documented, but this is the first report revealing the presence of the polymorphism in diazepam metabolism in rats. The current results infer polymorphic expression of new diazepam p-hydroxylating enzyme with lower Km than CYP2D1 in EM Wistar rats. © 2004 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci 93:1271–1278, 2004

Decreased mRNA Expression of the PTH/PTHrP Receptor and Type II Sodium-Dependent Phosphate Transporter in the Kidney of Rats Fed a High Phosphorus Diet Accompanied with a Decrease in Serum Calcium Concentration

This study investigates the phosphorus (P) homeostasis in the process of an altered parathyroid hormone (PTH) action in the kidney of rats fed a high P diet. Four-week-old male Wistar strain rats were fed diets containing five different P levels (0.3, 0.6, 0.9, 1.2 and 1.5%) for 21 days. The serum PTH concentration and urinary excretion of P were elevated with increasing dietary P level. Compared to rats fed the 0.3% P diet, the serum calcium (Ca) concentration remained unchanged, while the serum 1,25(OH)(2)D(3) concentration and urinary excretion of cAMP were elevated with increasing dietary P level in rats fed the high P diets containing 0.6-0.9% P. On the other hand, a lower serum Ca concentration was observed in rats fed the high P diets containing 1.2% or greater P. The serum 1,25(OH)(2)D(3) concentration remained unchanged in rats fed the high P diets containing 1.2% or greater P, comparison with rats fed the 0.3% P diet. The urinary excretion of cAMP and PTH/PTH-related peptide (PTHrP) receptor and type II sodium-dependent phosphate transporter (NaPi-2) mRNA in the kidney were both decreased in rats fed the high P diets containing 1.2% or greater P. In conclusion, a high P diet with subsequent decrease in serum Ca concentration suppressed the PTH action in the kidney due to PTH/PTHrP receptor mRNA down-regulation. Furthermore, an increase in the urinary excretion of P might have been caused by decreased NaPi-2 mRNA expression without the effects of PTH and 1,25(OH)(2)D(3).

Effect of intensive exercise-induced testicular gametogenic and steroidogenic disorders in mature male Wistar strain rats: a correlative approach to oxidative stress.

In order to investigate the effects of intensive exercise on reproductive dysfunctions in relation to oxidative stress, a total of 12 male rats (age: 3 months, weight: 127 +/- 2.86 g) were randomly divided into: (1) control group (CG, n = 6) and (2) experimental group (Exp. G, n = 6). An exercise protocol of 3 h swimming day(-1), 5 days week(-1) was followed for 4 weeks in Exp. G, with no exercise in CG. All the animals were killed; blood, testes and the accessory sex organs were collected for estimation of different parameters. A significant diminution (P < 0.001) was noted in testicular Delta5, 3beta-hydroxy-steroid dehydrogenase (Delta5, 3beta-HSD), 17beta-hydroxy steroid dehydrogenase (17beta-HSD); plasma levels of testosterone, luteinizing hormone (LH); preleptotine spermatocytes (pLSc), midpachytene spermatocytes (mPSc) and stage 7 spermatids (7Sd); with no significant alteration in follicle stimulating hormone (FSH) and spermatogoia A (Asg) after intensive exercise. A significant elevation (P < 0.001) in malondialdehyde (MDA) and conjugated dienes (CD) along with significant reduction (P < 0.001) in glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione-s-transferase (GST) and peroxidase were found in testes of Exp. G. Moreover, the somatic index of testes and accessory sex organs were also decreased significantly (P < 0.001) after exercise. High correlations have been found in 17 beta-HSD with CAT (r = 0.90, P < 0.05) and peroxidase (r = 0.83, P < 0.05), epididymal somatic index with CD (r = -0.91; P < 0.05) and GSH (r = 0.84, P < 0.05). The present study focused an chronic intensive exercise-induced oxidative stress that may cause dysfunctions in male reproductive system including steroidogenesis and spermatogenesis.

Lipoic acid as a rescue agent for adriamycin-induced hyperlipidemic nephropathy in rats

Adriamycin [ADR] is a cell independent model of glomerular injury. Hyperlipidemia associated with nephrotic syndrome may play a role in the deterioration of renal function. The study was carried out with adult male albino rats of Wistar strain comprising six rats in each group. Rats were fed with a standard rat pellet diet and were given access to water ad libitum. Group I rats served as controls (0.5 ml/day/rat i.p). Group II rats received ADR (1 mg/kg body weight/day) intravenously through the tail vein. Group III rats were given lipoic acid [LA] (35 mg/kg body weight/day) intraperitoneally. Group IV rats received LA 24 hours prior to the administration of ADR. ADR administered rats showed a significant increase ( p < 0.05) in serum lipids and lipoprotein fractions. However, the kidney of ADR administered rat showed a decline ( p < 0.05) in the content of phospholipids and free fatty acids. Significant ( p < 0.05) alterations were also observed in the activities of lipid metabolizing enzymes Pre-treatment with LA reverted the levels of lipid profiles and serum lipoproteins to near normal. The activities of lipid metabolizing enzymes also showed considerable changes on LA pre-treatment. This study highlights the antilipemic action of LA and its role as a protective agent for hyperlipidemia, associated with ADR induced nephrotic syndrome.

Expression of heat shock protein 72 in rat quadriceps muscles following anterior cruciate ligament resection

AbstractThis study investigated the expression of heat shock protein 72 (HSP 72) in quadriceps femoris muscle following anterior cruciate ligament (ACL) resection and running training in rats. A group of 15 Wistar strain male rats (10 weeks old) were divided into three groups: sham-operated (S), ACL resection (A), and running training following ACL resection (R). In the A and R groups, the ACL of the right knee was resected using microsurgical techniques. Rats in the R group were subjected to running training for 9 weeks on a motor-driven treadmill for rodents 1 week after ACL resection. At 10 weeks after ACL resection, glycerinated single fibers were prepared from vastus lateralis (VL), vastus medialis (VM), rectus femoris (RF), and semimembranosus (SM) muscles. To determine the levels of HSP72 (HSP- inducible) in each muscle, we used the Western blotting technique. HSP72 expression in VL and VM increased following ACL resection (P < 0.05) but not in RF or SM. Exercise training caused an elevation in HSP72 expression in VL and VM. There were no significant changes in HSP72 expression in RF or SM following exercise training. These results suggest that some stress would be generated by ACL resection in VM and VL and might cause atrophy in VM and VL.