Effect of benzene on the enzymes of carbohydrate metabolism, brush border membrane (BBM) and oxidative stress in kidney and other rat tissues

Abstract Benzene found all over our environment and are toxic to general population especially children. This aromatic hydrocarbon being used in making of rubbers, lubricants, drugs, dyes and used as intermediate to make other chemicals and thus cause occupational hazard. Studies were carried out exposing the adult Wistar rats of 175-200gm to benzene (800mg/ kg body weight) via gavaging in corn oil for a period of 30 days and control rats received only vehicle for same period. The aim of the present work was to study the effect of benzene on the enzyme of carbohydrate metabolism, BBM and antioxidant defense parameters in different rat tissues. The nephrotoxic effect of benzene was manifested by increase blood urea nitrogen, serum creatinine and cholesterol levels. The activity of lactate dehydrogenase (LDH) increases whereas malate dehydrogenase (MDH) was decreased by benzene. The biomarker of brush border membrane alkaline phosphatase, gamma-glutamyl tranferase and leucine amino peptidase decreased in BBM of rat tissues. The activity of gluconeogenic enzymes G6Pase and FBPase declined by benzene exposure. In addition, the activities of superoxide dismutase and catalase significantly decrease with associated increase in lipid peroxidation. The results indicate that benzene induced nephrotoxicity and lowered the enzymes of carbohydrate metabolism and BBM most likely by inducing oxidative stress

Studies on the protective effect of fish oil against cisplatin induced hepatotoxicity

Abstract Cisplatin (CP) is considered as a major antineoplastic drug against a broad spectrum of malignancies. The tissue specific toxicity of cisplatin to the kidneys is well documented. However, at higher doses less common toxic effects such as hepatotoxicity may arise. Although cisplatin remains one of the most effective antineoplastic drugs used in chemotherapy, strategies to protect tissues against cisplatin toxicity are of clinical interest. Dietary fish oil (FO) enriched in ω-3 fatty acids is known to retard the progression of certain types of cancers, cardiovascular and tissue disorders. In view of this, the present study investigates the protective effect of FO on CP induced damage to liver. Rats were pre-fed normal diet and the diet rich in FO for 10 days and then a single dose of CP (6mg/kg body weight) was administered intraperitoneally while still on diet. Serum/urine parameters, enzymes of carbohydrate metabolism and oxidative stress were analyzed. CP caused perturbation of the antioxidant defense as is reflected by the decrease in the activities of catalase, superoxide dismutase and glutathione peroxidase. Further the activities of various enzymes involved in glycolysis, TCA cycle, gluconeogenesis and HMP shunt pathway were determined and were found to be differentially altered by CP treatment. However, these alterations were ameliorated in cisplatin treated rats fed on fish oil. Present results show that dietary supplementation of FO to CP treated rats ameliorated CP-induced hepatotoxic and other deleterious effects due to its intrinsic biochemical/antioxidant properties

Thyroid hormone stimulation of Na/Pi-cotransport in opossum kidney cells.

Thyroid hormone (T3), a known stimulator of renal proximal tubular brush border membrane Na-dependent phosphate (Pi) uptake (Na/Pi-cotransport), stimulated Na-dependent Pi transport in opossum kidney (OK) cells. Na/Pi-cotransport was stimulated in a time- and dose-dependent manner with maximal effects (57%) at 24 h and 10(-10) M T3. This stimulation was related to an increase in the apparent capacity (Vmax) of Na/Pi-cotransport. Treatment with T3 had no effect on Na-independent transport of Pi or of L-arginine. The stimulation of Na/Pi-cotransport was paralleled by an increase in the messenger ribonucleic acid (mRNA) encoding the OK cell apical Na/Pi-cotransporter (termed NaPi-4); the mRNA levels related to the activity of Na-independent L-arginine transport (rBAT) were unaffected by T3. Actinomycin D (10(-7) M) completely prevented the stimulatory effect of T3 on OK cell Na/Pi-cotransport and on NaPi-4 mRNA content. In conclusion, T3 stimulates apical Na/Pi-cotransport in OK cells most likely by enhancing its transcription