Alla Gopala Reddy

The aim of this study is to evaluate the hepatoprotective effect of rutin (RTN) in comparison to silymarin (SLM) against acetaminophen (APAP)-induced hepatotoxicity in rats. Male Wistar albino rats (n=24) of 3 months age were equally divided into four groups. Group 1 served as normal control. Hepatotoxicity was induced in the remaining three groups with administration of 500 mg/kg po APAP from day 1-3. Groups 2, 3, and 4 were subsequently administered orally with distilled water, 25 mg/kg of SLM, and 20 mg/kg of RTN, respectively, for 11 days. The mean body weights and biomarkers of hepatotoxicity were estimated on day 0, 4 (confirmation of toxicity), and 15 (at the end of treatment). Hematological parameters were evaluated on day 4 and 15. Antioxidant profile and adenosine triphosphatases (ATPases) were assessed at the end of the experiment. Liver tissues were subjected to histopathology and transmission electron microscopy after the sacrifice on day 15. Antioxidant profile, ATPases, and hematological and sero-biochemical parameters were significantly altered, and histopathological changes were noticed in the liver of toxic control group. These changes were reversed in groups 3 and 4 that were administered with SLM and RTN, respectively. The results of the present investigation enunciated that SLM has potent hepatoprotective activity though the RTN was found superior in restoring the pathological alterations in paracetamol-induced hepatotoxicity in Wistar albino rats.

The incidence of esophageal cancer is rapidly increasing especially in developing countries. The major risk factors include unhealthy lifestyle practices such as alcohol consumption, smoking, and chewing tobacco to name a few. Diagnosis at an advanced stage and poor prognosis make esophageal cancer one of the most lethal diseases. These factors have urged further research in understanding the pathophysiology of the disease. Animal models not only aid in understanding the molecular pathogenesis of esophageal cancer but also help in developing therapeutic interventions for the disease. This review throws light on the various recent laboratory animal models for esophageal cancer.

The objective of the study was to assess the effect of combination treatment of insulin, pioglitazone and synbiotic on streptozotocin (STZ)-induced diabetic rats. Diabetes mellitus was induced chemically by intraperitoneal administration of STZ (40 mg/kg b.wt) to male Sprague-Dawley rats. The rats were divided randomly into six groups of six rats in each. Group 1 was maintained as a normal control. Group 2 was maintained as diabetic control; Group 3 was treated with insulin; Group 4 with insulin + synbiotic; Group 5 with insulin + pioglitazone; and Group 6 with insulin + synbiotic + pioglitazone. All the animals were treated for 60 days. Body weights, and concentration of reduced glutathione (GSH), and high-density lipoproteins cholesterol were significantly (p<0.05) reduced, whereas the concentration of blood glucose, total cholesterol, triglycerides, protein carbonyls and thiobarbituric acid reacting substances, and the activity of GSH peroxidase were significantly (p<0.05) elevated in Group 2 at the end of 8(th) week as compared to Group 1. The treatment Groups 3, 4, 5 and 6 revealed improvement in all the parameters, and the highest improvement was observed in combination Group 6. From this study, it is concluded that combination of insulin, pioglitazone and synbiotic is useful in treating diabetes.

The study revealed higher values (t1/2, MRT and Vdss) of GL in curcumin pre-treated group due to the inhibitory effect of curcumin on intestinal CYP3A4.

The present study was conducted to assess the effect of fenugreek, insulin and glimepiride alone and their combination in diabetic rat liver. Fifty six male Sprague dawley rats of uniform age were randomly divided into seven groups. Group 1: Non-diabetic control; Group 2: Streptozotocin (40 mg/Kg i/p single dose)-induced diabetic control; Group 3: Insulin (4 U/kg once daily for 8 weeks) treatment in diabetic rats; Group 4: Glimepiride (4 mg/Kg orally once daily for 8 weeks) treatment in diabetic rats; Group 5: Fenugreek seed powder treatment (1 g/kg orally once daily for 8 weeks) in diabetic rats; Group 6: Insulin + Fenugreek seed powder treatment (once daily for 8 weeks) in diabetic rats; Group 7: Glimepiride + Fenugreek seed powder treatment (once daily for 8 weeks) in diabetic rats. Livers were collected at the end of experiment for histopathology and estimation of reduced glutathione (GSH), thiobarbituric acid reacting substances (TBARS), protein carbonyls, glutathione S-transferase (GST), glucose-6-phosphate dehydrogenase (G6PD), Na ⁺ /K ⁺ ATPase and Mg ²+ ATPase, cytochrome P ₄₅₀ (CYP) and glycogen. There was an increase in the concentration of TBARS and protein carbonyls, and decrease in the concentration of GSH and glycogen, and the activity of GST, G6PD, Na ⁺ /K ⁺ ATPase and Mg ²+ ATPase in diabetic livers, while treatment groups showed significant ( P < 0.05) increase in the above parameters. The histology of liver revealed marked changes in diabetic rats and mild changes in combination treatment groups. The treatment with fenugreek, insulin and glimepiride improved the liver parameters in diabetic rats and their combination showed a beneficial effect on liver.

The present study was aimed to investigate whether α-tocopherol could protect the chromium (Cr) VI-induced oxidative stress in female reproductive system of rats and to explore the underlying mechanisms of the same. A total of 24 Wistar adult female rats were equally divided into four groups. Group 1 served as control, while groups 2 and 3 were administered K ₂ Cr ₂ O ₇ (10 mg/kg b.wt. s.c. single dose). In addition to Cr, group 3 also received α-tocopherol @ 125 mg/kg daily by oral gavage for 14 days. Group 4 was maintained as α-tocopherol control (dose as above). Body weights were recorded at the beginning and at the end of experiment. Further, the rats were observed for occurrence of estrus cycle. At the end of 14 days, blood samples were drawn for sero-biochemical analysis. Subsequently, all the rats were sacrificed to collect uterus along with ovaries for assay of tissue peroxidation, anti-oxidant and functional markers, and histopathology. Administration of chromium (Cr) VI to rats revealed a significant (P < 0.05) accumulation of cholesterol and a prolonged diestrus phase leading to impaired fertility in rats. Administration of chromium (Cr) VI significantly ( P < 0.05) reduced the antioxidant markers such as superoxide dismutase (SOD) and reduced glutathione (GSH), along with significant ( P < 0.05) increase in peroxidation markers such as malondialdehyde and protein carbonyls in ovaries. The functional marker in serum such as total protein was decreased, whereas other functional markers viz alanine transaminase (ALT), blood urea nitrogen (BUN) and creatinine were increased. Prominent pathological changes were observed in the uterus and ovaries of Cr-treated group. Co-treatment with α-tocopherol significantly (P < 0.05) reversed the (Cr) VI induced changes.

In the present study, the effects of oral administration of imidacloprid for 4 weeks on serum biochemical, oxidative stress, histopathological and ultrastructural alterations were assessed in the liver of male rats. This study also aimed to investigate whether vitamin C could protect against the imidacloprid-induced oxidative stress. Forty-eight male Sprague dawley rats were divided into four groups of 12 animals each. Group 1 served as the control, while groups 2 and 4 were administered with imidacloprid (80 mg/kg body weight) daily by oral gavage for 28 days. In addition to imidacloprid, group 4 also received vitamin C at 10 mg/kg daily by oral gavage for 28 days. Group 3 was maintained as the vitamin C control (dose as above). The serum biochemical assays revealed a significant ( P < 0.05) increase in alanine transaminase and aspartate transaminase and decrease in total protein in group 2. The tissue biochemical profile revealed a significant ( P < 0.05) reduction in reduced glutathione concentration in the liver of group 2 animals. Histologically, the liver showed marked dilation, congestion of central vein, portal vein and sinusoidal spaces, vacuolation/fatty change and degenerated hepatocytes. Ultra thin sections of the liver revealed swollen nuclei, varied size and shape of mitochondria, disrupted chromatin and rough endoplasmic reticulum. Co-treatment with vitamin C significantly ( P < 0.05) reversed the imidacloprid-induced changes.

Introduction : One of the target organs of heavy metals is testis and many authors proposed that oxidative stress could be responsible to induce their toxicity. An experimental study was conducted to evaluate the molecular mechanisms of lead (Pb) and cadmium (Cd) toxicity, their toxicodynamic interaction and to evaluate therapeutic potential of N-Acetyl L-cysteine (NAC) against the reproductive toxicity in male Wistar rats. Material and methods : rats were randomly divided into 8 groups comprising of 6 rats in each. Group 1 and 2 were syam and NAC control, Group 3, 4 and 5 were kept as toxic control groups such as lead, cadmium and lead + cadmium respectively, where as Group 6, 7 and 8 were therapeutic groups with NAC. The experiment scheduled for 3 months. Body weights, anti-oxidant profile (GSH, GST, TBARS and protein carbonyls) in testis, testis weight, testicular LDH, sperm count and histopathology were conducted. And also, interaction of Pb and Cd with zinc (Zn) and copper (Cu) in testis was assessed. Results : The present study revealed significant alterations in body weights, anti-oxidant profile, weights of testes, testicular LDH, sperm count, and concentration of Zn and Cu in toxic control groups 3, 4 and 5 as compared to control and NAC-treated groups. The toxic combination (Pb+Cd) group 5 showed significant alterations in protein carbonyls, GST levels and testicular LDH as compared to Pb and Cd alone administered groups and these results are substantiated with marked changes in the histopathology. All the NAC-treated groups revealed significant improvement in all the parameters. Conclusion : The results of the investigation revealed that Pb, Cd and their combination induces toxicity to the biological system due to the excess generation of free radicals and impairment of anti-oxidant defenses. Toxic effects were more pronounced in the group that received a combination of Pb and Cd, suggesting positive toxicodynamic interaction. Use of NAC countered the adverse effects of Pb and Cd induced toxicity to a major extent suggesting its anti-oxidant potential owing to replenishment of tissue pool of GSH. Further, NAC administration reduced the extent of accumulation of Pb and Cd in various tissues.

Objective : The present study was aimed to study protective role of N-acetyl cysteine (NAC) was assessed against arsenic (As)-induced hepatotoxicity in rats. Methods : Twenty four male Wistar rats were divided into 4 groups of 6 animals each and treated as follows: Group 1: sham control, 2: arsenic control (sodium arsenite @ 10 mg/kg b. wt orally for 4 wks), 3: Pre-treatment with NAC (@ 300 mg/kg orally for 2 wks) followed by sodium arsenite along with NAC (as per above doses) and 4: Sodium arsenite + NAC (as per above doses for 4 wks). Results : The concentration of thiobarbituric acid reacting substances (TBARS) and protein carbonyls was significantly (PP<0.05) reduced in group 2 as compared to control. Groups 3 and 4 revealed improvement in the parameters in study. Conclusion : The study revealed that arsenic induces hepatotoxicity by inducing oxidative stress and supplementation of NAC is beneficial in countering the adverse effects.