Inhibitory effects of Zinc on hyperglycaemia and metabolic disorders in the liver of alloxan-induced diabetic rats

Background: Zinc may participate as a component of the antioxidant defense system. Its deficiency induces oxidative damage to cell components and alterations in antioxidants enzymes in both animal and cells models. There are few studies to provide evidence of the action of zinc in diabetic animal models. Objective: To evaluate the action of oral administration of zinc (Zn) in hyperglycemia and metabolic disorders induced in the liver of alloxan-induced diabetic rats. Materials and method: Wistar rats (age: two months) were used for this study. Inducing diabetes in rats using alloxan, we obtained the diabetic rats after four weeks. The rats were divided into five groups (each n=8): normal (control) rat, diabetic rats before the beginning of treatment (Diab-ref), diabetic rats at the end of the treatment (Diab-Con), diabetic rats treated with zinc gluconate (Diab+Zn), and diabetic rats treated with insulin (Diab+Ins). Zinc was orally administrated in drinking water at dose 150mg/L, and insulin was administrated at 0.5IU/rat/day. Thiobarbituric acid-reactive substances (TBARS) superoxide dismutase (SOD), glutathione peroxidise (GPX), catalase (CAT), transaminase glutanic pyruvic (TGP), transaminase glutanic oxaloacetic (TGO), total bilirubin, total cholesterol (TCh), triglyeerides (TG), high density lipid-cholesterol (HDL-Ch), plasmatic, and liver glucose were determined in blood and liver samples. Results: Zn administration significantly decreased glucose level and glycogen content. Activities of SOD, CAT and GPO were significantly increased by Zn-treatment. In addition, the liver toxicity was prevented by significantly lowering in total bilirubin, TARSs, TGP, and TPO. Conclusion: Zinc supplements may be beneficial for correcting hyperglycemia leading to diabetic complications in the liver.

Inhibitory effect of estrogens, phytoestrogens, and caloric restriction on oxidative stress and hepato-toxicity in aged rats / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate the protective effect of 17beta-estradiol (E2), peganum harmala extract (PHE) administration and calorie restriction (CR) treatment (60%) on oxidative stress and hepato-toxicity in aged rats.</p><p><b>METHODS</b>Eighteen months old animals that were treated at the age of 12 months were divided into 4 groups: normal control group with free access to food, E2 treatment group, PHE treatment group and CR treatment group of the food given to control group. Six male rats at the age of 4 months were used as a reference group.</p><p><b>RESULTS</b>Aging significantly decreased superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX), and increased lactate deshydrogenase (LDH), gamma-glytamyl transferase (GGT), phosphatase alkalines (PAL), aspartate and lactate transaminase (AST and ALT) activities in the liver. Aging also induced an increased lipid peroxidation level, histological changes and a decreased E2 level. However, treatment with E2, PHE, and CR increased 17beta-estradiol, and decreased hepatic dysfunction parameters and lipid peroxidation as well as histological changes in the liver of aged rats.</p><p><b>CONCLUSION</b>The antioxidant and hepatoprotective activity of PHE and CR is possibly attributed to its ability to increase E2 level, which as an antioxidant, acts as a scavenger of ROS. Further studies on the pharmaceutical functions of E2 in males may contribute to its clinical application.</p>

Protective effects of estrogens and caloric restriction during aging on various rat testis parameters / 亚洲男科学杂志(英文版)

<p><b>AIM</b>To investigate the effects of 17beta-estradiol (E2), Peganum harmala extract (PHE) and caloric restriction (CR) on various testis parameters during aging.</p><p><b>METHODS</b>Twelve month-old male rats were treated for 6 months with either E2 or PHE, or submitted to CR (40%).</p><p><b>RESULTS</b>Our results show that estrogens and CR are able to protect the male gonad by preventing the decrease of testosterone and E2 levels as well as the decrease of aromatase and estrogen receptor gene expressions. Indeed, E2, PHE and CR treatments induced an increase in the superoxide dismutase activities and decreased the activity of testicular enzymes: gamma-glutamyl transferase, alkaline phosphatase, lactate deshydrogenase as well as the aspartate and lactate transaminases in aged animals. In addition, the testicular catalase and gluthatione peroxidase activities were enhanced in E2, PHE and CR-treated rats compared to untreated animals at 18 months of age. Moreover, the positive effects of estradiol, PHE and CR were further supported by a lower level of lipid peroxidation. Recovery of spermatogenesis was recorded in treated rats.</p><p><b>CONCLUSION</b>Besides a low caloric diet which is beneficial for spermatogenesis, a protective antioxydant role of estrogens is suggested. Estrogens delay testicular cell damage, which leads to functional senescence and, therefore, estrogens are helpful in protecting the reproductive functions from the adverse effects exerted by reactive oxygen species (ROS) produced in large quantities in the aged testis.</p>

Age-related decrease in aromatase and estrogen receptor (ERalpha and ERbeta) expression in rat testes: protective effect of low caloric diets / 亚洲男科学杂志(英文版)

<p><b>AIM</b>To examine the effects on rat aging of caloric restriction (CR1) and undernutrition (CR2) on the body and on testicular weights, on two enzymatic antioxidants (superoxide dismutase and catalase), on lipid peroxidation and on the expression of testicular aromatase and estrogen receptors (ER).</p><p><b>METHODS</b>CR was initiated in 1-month-old rats and carried on until the age of 18 months.</p><p><b>RESULTS</b>In control and CR2 rats an age-related decrease of the aromatase and of ER (alpha and beta) gene expression was observed; in parallel a diminution of testicular weights, and of the total number and motility of epididymal spermatozoa was recorded. In addition, aging in control and CR2 rats was accompanied by a significant decrease in testicular superoxide dismutase, catalase activities, and an increase in lipid peroxidation level (thiobarbituric acid reactive substance), associated with alterations of spermatogenesis. Conversely, caloric restriction-treatment exerted a protective effect and all the parameters were less affected by aging.</p><p><b>CONCLUSION</b>These results indicate that during aging, a low caloric diet (not undernutrition) is beneficial for spermatogenesis and likely improves the protection of the cells via an increase of the cellular antioxidant defense system in which aromatase/ER could play a role.</p>