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Sodium nitrite (SNT) widely used as a curative agent in meat processing industry possesses cell-transforming mutagenic and cytogenic properties. Dietary omega-3 polyunsaturated fatty acids (ω-3 PUFA) has been shown to reduce the severity of certain types of cancers, cardiovascular and renal diseases. The present study examined whether feeding of fish oil (FO)/flaxseed oil (FXO) has protective effect against SNT-induced toxicity. SNT significantly altered the activities of serum creatinine (Crt), blood urea nitrogen (BUN), metabolic and brush border membrane (BBM) enzymes. SNT caused significant imbalances in the antioxidant system associated with increased lipid peroxidation (LPO). Feeding of FO and FXO with SNT ameliorated the changes in various parameters caused by SNT. Nephrotoxicity parameters lowered and enzyme activities of carbohydrate metabolism, BBM and radioactively labeled inorganic phosphate (32Pi) transport were improved to near control values. The results of the present study suggest that ω-3 PUFA-enriched FO and FXO from sea-foods and plant sources respectively are similarly effective in reducing SNT-induced nephrotoxicity and oxidative damage.

The effect of ischemia induced acute renal failure (ARF) on the transport of phosphate (Pi) after early (15–30 min) and prolonged (60 min) ischemia in the brush border membrane vesicles (BBMV) from rat renal cortex was studied. Sodium-dependent transport of Pi declined significantly and progressively due to ischemia. Western blot analysis of BBM from ischemic rats showed decreased expression of NaPi-2. A compensatory increase was observed in Pi uptake in BBMV from contralateral kidneys. There was no significant difference in NaPi-2 expression between BBMV from sham and contralateral kidneys. Early blood reperfusion for 15 min after 30 min ischemia caused further decline in Pi uptake. Prolonged reperfusion for 120 min caused partial reversal of transport activities in 30-min ischemic rats. However, no improvement in the transport of Pi was observed in 60-min ischemic rats after 120 min of blood reperfusion. Kinetic studies showed that the effect of ischemia and blood reperfusion was dependent on the V max of the Na-Pi transporter. Western blot analysis showed increased expression of NaPi-2 in the BBMs from ischemia–reperfusion animals. Further, a shift in the association of Na ions to transport one molecule of Pi was observed under different extracellular Na concentrations [Na] o . Feeding rats with low Pi diet and/or treatment with thyroid hormone (T3) prior to ischemia resulted in increased basal Pi transport. Ischemia caused similar decline in Pi transport in BBM from LPD and/or T3 animals. However, recovery in these animals was faster than the normal Pi diet fed (NPD) animals. The study suggests a change in the intrinsic properties of the Na-Pi transporter in rat kidneys due to ischemia. The study also indicates that treatment with T3 and feeding LPD prior to ischemia caused faster recovery of phosphate uptake due to ischemia–reperfusion injury.