Zinc oxide nanoparticles augment CD4, CD8, and GLUT-4 expression and restrict inflammation response in streptozotocin-induced diabetic rats.

This study evaluated the biochemical, molecular, and histopathological mechanisms involved in the hypoglycaemic effect of zinc oxide nanoparticles (ZnONPs) in experimental diabetic rats. ZnONPs were prepared by the sol-gel method and characterised by scanning and transmission electron microscopy (SEM and TEM). To explore the possible hypoglycaemic and antioxidant effect of ZnONPs, rats were grouped as follows: control group, ZnONPs treated group, diabetic group, and diabetic + ZnONPs group. Upon treatment with ZnONPs, a significant alteration in the activities of superoxide dismutase, glutathione peroxidase, and the levels of insulin, haemoglobin A1c, and the expression of cluster of differentiation 4+ (CD4+), CD8+ T cells, glucose transporter type-4 (GLUT-4), tumour necrosis factor, and interleukin-6 when compared to diabetic and their control rats. ZnONPs administration to the diabetic group showed eminent blood glucose control and restoration of the biochemical profile. This raises their active role in controlling pancreas functions to improve glycaemic status as well as the inflammatory responses. Histopathological investigations showed the non-toxic and therapeutic effect of ZnONPs on the pancreas. TEM of pancreatic tissues displayed restoration of islets of Langerhans and increased insulin-secreting granules. This shows the therapeutic application of ZnONPs as a safe anti-diabetic agent and to have a potential for the control of diabetes.

Prominent free radicals scavenging activity of tannic acid in lead-induced oxidative stress in experimental mice.

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.

Role of selenium on antioxidant capacity in methomyl-treated mice

Methomyl carbamate is a pesticide widely used in the control of insects. The presentwork aims at studying the effect of selenium on the antioxidant system ofmethomyl-treated mice. Swiss albino mice were intraperitoneally administered a singledose of methomyl (7 mg/Kg body weight). Mice of another group were injectedwith sodium selenite (5 µmole/Kg b.wt.) 7 days before methomyl intoxication. After24 hours, methomyl exposure resulted in significant increase in lactic dehydrogenaseactivity (LDH). The antioxidant capacity of hepatic cells in terms of the activities ofsuperoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione-S-transferase (GST) and glutathione (GSH) content was diminished. Itappears that methomyl exerts its toxic effect via peroxidative damage to hepatic, renaland splenic cell membranes. Also, methomyl induced DNA damage in these organsas detected by alkaline filter elution technique. The distribution of methomyl in differentorgans of mice was detected by HPLC. Selenium administration prior tomethomyl injection produced pronounced protective action against methomyleffects. It is observed that selenium enhances the endogenous antioxidant capacity ofthe cells by increasing the activities of SOD, CAT, GR and GST as well as increasingGSH content. The activity of LDH was decreased in blood and the damage ofDNA was suppressed comparable to controls. In conclusion, the adverse effects ofmethomyl in mice could be ameliorated by selenium

Role of selenium on antioxidant capacity in methomyl-treated mice.

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.

Protective role of Egyptian propolis against tumor in mice.

BACKGROUND: Propolis has numerous biologic activities including antibiotic, antifungal, antiviral and anti-inflammatory properties. The present work is aimed to study the effect of crude Egyptian propolis on tumor in mice induced by Ehrlich ascitis carcinoma (EAC) cell line. RESULTS: The administration of propolis (160 mg/kg body weight), by gastric intubation 2 h before the intraperitoneal injection of EAC, effectively inhibited tumor growth and the proliferation of EAC. The tumor volume was markedly reduced from 7+/-0.9 ml in EAC-infected mice to 1.6+/-0.95 ml in propolis-treated mice. Also, the lipid peroxide level which was 13.3+/-1.24 nmol malodialdehyde (MDA)/mg protein in EAC infected mice was significantly decreased to 3.3+/-2.1 nmol MDA/mg protein. Reduced glutathione (GSH) and glutathione S-transferase (GST) concentrations were markedly increased in propolis-treated mice. This effect was associated with inhibition of cell cycle progression and induction of apoptosis. Administration of propolis 2 h before injection of EAC arrested cells in G0/G1 phase and resulted in a decrease in the viability, DNA, total RNA and protein level of tumor cells. CONCLUSIONS: Crude Egyptian propolis has a strong inhibitory activity against tumors. The anti-tumor mechanism may be mediated by preventing oxidative damage and induction of apoptosis.

Protective action of copper (II) complex of a Schiff base against DNA damage induced by m-chloroperbenzoic acid using a novel DNA unwinding technique.

DNA strand breaks can be detected with great sensitivity by exposing calf thymus DNA to alkaline solutions and monitoring the rate of strand unwinding. Fluorometric analysis of DNA unwinding (FADU) is a reliable method for detecting single-strand DNA breaks as an index of DNA damage induced by photosensitizer.m-Chloroperbenzoic acid (CPBA) was used as a photosensitizer in the photodamage of calf thymus DNA. When DNA is exposed to ionizing radiation, the radicals produced in the irradiated sample modify the base-pair regions of the double strands. The protective action of copper salt, Schiff base [ethylene diamine with ethyl acetate](L) and its Cu(II) complex (Cu(7) L Cl(14)) against DNA damage photoinduced by CPBA was studied using ethidium bromide as a fluorescent probe. Treatment of DNA with 5, 10, 50, 100, or 200 microM CPBA produced 75%, 48%, 38%, 32% and 30% double-stranded DNA remaining, respectively after 30 min of alkaline treatment at 15 degrees C. Treatment of calf thymus DNA irradiated with CPBA with a dose of 1 mM [Cu(7) L Cl(14)] produced 96% double-stranded remaining protection under the same conditions compared with irradiated DNA without addition of Cu(II) complex of Schiff base.