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给大鼠腹注五氧化二钒(V_2O_5)10mg/kg,每天一次,连续四天,导致明显肾脏损害。染毒两天后,出现尿量、尿钠与钾排泄、尿糖以及尿中ALP、LDH、GOT、GPT酶活性增加;血糖和尿渗透浓度降低。染毒四天后,除上述改变外,还出现尿蛋白、血肌酐和尿素氮增高。主要病理学改变为肾近曲小管细胞变性和坏死。用醋酸锌作为保护剂研究肾损害与脂质过氧化的关系,结果表明,大鼠用锌预处理后,V_2O_5诱导的脂质过氧化和急性肾损同时减轻。提示 V_2O_5诱导的脂质过氧化可能是形成肾损害的机理之一。
Rats were given an intraperitoneal injection of vanadium pentoxide (V_2O_5) 10 mg/kg once daily for four consecutive days, leading to significant kidney damage. Two days after exposure, urine output, urinary sodium and potassium excretion, urine glucose, and urinary ALP, LDH, GOT, GPT enzyme activity increased; blood glucose and urine osmolality decreased. Four days after exposure, in addition to the above changes, there were also increases in urine protein, serum creatinine, and urea nitrogen. The main pathological changes were renal proximal tubular cell degeneration and necrosis. Zinc acetate was used as a protective agent to study the relationship between renal damage and lipid peroxidation. The results showed that V_2O_5-induced lipid peroxidation and acute renal injury were alleviated in rats pretreated with zinc. It is suggested that lipid peroxidation induced by V_2O_5 may be one of the mechanisms of renal damage.