Hypocalcemia increases the nephrotoxic effects of ammonium molybdate

Abstract

Objective. One of the pathogenic mechanisms of heavy metals cytotoxic action is the disruption of calcium homeostasis. The calcium in the body may take part in competitive relationship with heavy metals and influence on their metabolism. In this regard, the aim of the research was to study the peculiarities of renal function changes under the action of molybdenum in conditions of hypocalcemiamodels. Methods. In the experiment on Wistar rats the effect of calcitonin on the renal manifestations of intoxication caused by the introduction of ammonium molybdate was investigated. Calcitonin was injected daily subcutaneously at a dosage of 0.6 U/100 g body weight for 20 days, an hour later calcitonin unjection ammonium molybdate was administered parenterally at a dosage of 50 mg/kg (in recalculation on metal) 1 time per day. At the end of the experiment animals were killed under thiopental anesthesia. Results. It was found that ammonium molybdate caused more pronounced changes in renal function under conditions of hypocalcemia in the form of polyuria due to the reduced tubular reabsorption of water, despite of the decrease in glomerular filtration rate. At the same time more pronounced proteinuria was noted. The study ion-excretory renal function showed the reduction of sodium tubular reabsorption and its increased urinary excretion, at a reduced filtration charge. Excretion and filtration of potassium was increased. Calciuresis was increased with reduced filtration charge. Electrolyte composition of blood plasma was characterized by low sodium and high calcium and potassium levels. Conclusion. The study revealed that hypocalcemia enhanced the toxic effect of ammonium molybdate on renal function.