No abstract

Methomyl carbamate is a pesticide widely used in the control of insects. The present work aims at studying the effect of selenium on the antioxidant system of methomyl-treated mice. Swiss albino mice were intraperitoneally administered a single dose of methomyl (7 mg/Kg body weight). Mice of another group were injected with sodium selenite (5 pmole/Kg b.wt.) 7 days before methomyl intoxication. After 24 hours, methomyl exposure resulted in significant increase in lactic dehydrogenase activity (LDH). The antioxidant capacity of hepatic cells in terms of the activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione-S-transferase (GST) and glutathione (GSH) content was diminished. It appears that methomyl exerts its toxic effect via peroxidative damage to hepatic, renal and splenic cell membranes. Also, methomyl induced DNA damage in these organs as detected by alkaline filter elution technique. The distribution of methomyl in different organs of mice was detected by HPLC. Selenium administration prior to methomyl injection produced pronounced protective action against methomyl effects. It is observed that selenium enhances the endogenous antioxidant capacity of the cells by increasing the activities of SOD, CAT, GR and GST as well as increasing GSH content. The activity of LDH was decreased in blood and the damage of DNA was suppressed comparable to controls. In conclusion, the adverse effects of methomyl in mice could be ameliorated by selenium.

Lead (Pb) is known to disrupt the pro-oxidant/antioxidant balance of tissues leading to biochemical and physiological dysfunction. The present study was designed to investigate the effect of tannic acid on some biochemical parameters in Swiss albino mice exposed to lead acetate. The levels of thiobarbaturic acid-reactive substances (TBARS) as an index of lipid peroxidation, nitric oxide (NO), and serum lead (Pb) were significantly increased following intragastric administration of 50 micromole lead acetate/kg body weight three times a week, every other day for three weeks, compared to the corresponding control values. On the other hand, the activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione-S-transferase (GST) and glutathione content (GSH) and serum copper (Cu) and zinc (Zn) were significantly diminished relative to the control values. The administration of 20 mg tannic acid/kg body weight three times a week every other day for three weeks, enhanced the endogenous antioxidant capacity of the cells by increasing the activities of antioxidant enzymes (SOD, CAT, GSH-R, GST), GSH content and serum Cu and Zn levels. Compared to the lead acetate-exposed group, the levels of TBARS, NO and Pb were decreased in the lead acetate exposed group treated with tannic acid. These results afford evidence supporting the hypothesis that lead induces oxidative stress in hepatic cells. Moreover, tannic acid has a potential in sustaining global antioxidant effect in hepatic cells leading to decreased oxidative stress and cellular damage initiated through free radical production by lead acetate.

In many types of malignancy, ascites is a prognostic sign of advanced stage, with a survival rate of 11% for patients with ascites more than 6 months. Currently, combination therapy has become the base of cancer treatment. However, cytotoxicity to normal tissue is the major limitation of current combined drugs. In this study, Ehrlich ascites carcinoma (EAC) inoculated into mice was targeted with three consecutive doses of metformin, a safe drug with an anti-cancer effect. To test its suitability as a potential safe candidate against EAC cells for later combination therapy in comparable with cisplatin as a reference anti-neoplastic drug. The group that received metformin developed less malignant ascites than the control group. Metformin induced cellular quiescence in the EAC cells by upregulation of cyclin-dependent kinase inhibitor 1 (p21) expressions as cisplatin acted. Cell cycle analysis confirmed the quiescence state of the EAC cells treated with metformin or cisplatin. Furthermore, metformin-induced toxicity to EAC cells through elevation of reactive oxygen species levels (ROS). Therefore, metformin can be a suitable candidate for future combination with a low dose of cisplatin to treat the aggressiveness of EAC cells.

The purpose of the study is to investigate the role of sex hormones, androgen receptors (ARs) and miRNA/CSF-1 in occurrence and recurrence of calcium oxalate (CaOx) renal urolithiasis. In this prospective study, 74 patients with CaOx stones; stone formers group (SFG) and 40 healthy subjects; control group were compared. SFG includes both de novo and recurrent cases. Steroid sex hormone plasma assay including testosterone, free testosterone, dihydrotestosterone, estradiol, and sex hormone binding globulin was analyzed. ARs, miRNA-185-5p and CSF-1 expression were compared between the groups. SFG showed significant higher ARs and miRNA-185-5p expression (3.7 ± 1.3, 1.8 ± 0.4, respectively) than control group (1 ± 0.08 and 1 ± 0.07, respectively) (p < 0.05). However, CSF-1 expression was significantly lower in stone formers than control group (0.4 ± 0.19 vs 1 ± 0.1, respectively) (p < 0.05). No differences were detected between de novo and recurrent SFG regarding sex hormones, AR, miRNA or CSF-1 expression. Our data suggest the important role of AR, miRNA and CSF-1 signaling in human nephrolithiasis pathogenesis.