Study on activities and protein and gene expression of renal H(+)-K(+)-ATPase in rats subchronic exposed to trimethyltin chloride / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the activity, protein and gene expression of renal HK-ATPase (HKA) in rats subchronic exposed to trimethyltin chloride (TMT).</p><p><b>METHODS</b>In subchronic toxic test (14-week), 55 female SD rats (age, 6 weeks) were divided randomly into 5 groups: control, low, medium, high and super high dosage, respectively, which drank water with TMT of 0, 8.20, 32.81, 131.25 and 262.50 microg x kg(-1) x d(-1) for 14 weeks. Then serum K+ levels were measured; the activities of HK-ATPase (HKA) in kidneys were detected by the method of determinated phosphorus content; Western Blot assay and real-time PCR were used to exam the protein and mRNA expression levels of HKA in kidneys, respectively.</p><p><b>RESULTS</b>The serum K+ level in super-high dosage group was (5.6 +/- 0.4) mmol/L, which was significantly lower than that [(6.9 +/- 0.3) mmol/L] in control group (P < 0.01). The HKA enzymatic activity of kidneys in low and super high dosage groups was 4.50 +/- 1.45 and 4.55 +/- 0.72 micromolPi x mg prot(-1)h(-1), respectively, which were significantly lower than that (6.55 +/- 0.77 micromol Pi x mg prot(-1) h(-1)) in control group (P < 0.05).</p><p><b>CONCLUSION</b>When rats were exposed subchronic to TMT, the renal HKA activity could reduce, but the expression levels of HKA protein and mRNA did not decrease.</p>

Studies on hypokalemia induced by trimethyltin chloride / 生物医学与环境科学（英文）

<p><b>OBJECTIVES</b>To determine the possible relationship between plasma potassium concentration and severity of acute trimethyltin chloride (TMT) poisoning and to assess the mechanism of TMT induced hypokalemia.</p><p><b>METHODS</b>SD rats were treated with various dosages of TMT (i.p.). All the indices were measured and analysed for determining their possible relations with plasma K+.</p><p><b>RESULTS</b>With increase of dosage, the plasma K+ level dropped rapidly, and deaths appeared more quickly. The LD50 of TMT (i.p.) was 14.7 mg/kgbw. In the low dosage group (10 mg/kgbw), the plasma K+ level dropped slowly with the lowest dosage on day 6 (4.85 mmol/L). It rose again on day 11 (5.06 mmol/L), and recovered on day 28. The poisoning signs corresponded with decline of the span of K+ level. The plasma Na+ level dropped half an hour after TMT treatment, but recovered 24 h later. In the high dosage group (46.4 mg/kgbw), the levels of plasma K+ and Na+ fell rapidly within half an hour (P < 0.05), the intracellular potassium concentration of RBC did not decrease obviously (P > 0.05), the activities of Na(+)-K(+)-ATPase and Mg(2+)-ATPase in RBC membrane were depressed remarkably (P < 0.01, P < 0.05, respectively), the plasma aldosterone concentrations rose as high as tenfold (P < 0.01), the arterial blood pH fell from 7.434 to 7.258 (P < 0.01), pCO2 was raised from 29.62 to 45.33 mmHg (P < 0.01). In the 24 h urine test, when rats were treated with TMT (21.5 mg/kgbw, i.p.), urine volume, urinary potassium, sodium and chloride increased significantly in comparison with those in the controls (P < 0.01).</p><p><b>CONCLUSION</b>TMT could induce hypokalemia in SD rats. The available evidence suggests that TMT can induce acute renal leakage of potassium. At the same time, a significant rise of plasma aldosterone may play an important role in promoting potassium leakage from kidney to result in severe hypokalemia with inhaling acid-base abnormalities produced, which aggravate the poisoning symptoms. In the end the rats would die of respiratory failure.</p>