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N-苄基-D-葡糖胺二硫代氨基甲酸盐对大鼠无机汞肾毒性的影响。

Effect of N-benzyl-D-glucamine dithiocarbamate on renal toxicity of inorganic mercury in rats.

作者信息

Shimada H, Kiyozumi M, Kojima S

机构信息

Department of Hygienic Chemistry, Faculty of Pharmaceutical Sciences, Kumamoto University, Japan.

出版信息

Chem Pharm Bull (Tokyo). 1990 May;38(5):1429-31. doi: 10.1248/cpb.38.1429.

Abstract

The effect of N-benzyl-D-glucamine dithiocarbamate (BGD) on the renal toxicity of inorganic mercury in rats was studied. Rats were injected i.v. with saline or HgCl2 (300 micrograms Hg/kg) and 30 min later they were injected i.p. with saline or BGD (2778 mumol/kg, a quarter of an LD50). Urinary excretion of gamma-glutamyl-transpeptidase (gamma-GTP), which is a brush border enzyme, in rats after mercury treatment significantly increased compared to that of the control in the 12-24 h urine specimen and reached a maximum value within 24 h after the treatment. Urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG), which is a lysosomal enzyme, also significantly increased after mercury treatment compared to that of the control in the 12-24 h urine specimen and reached a maximum value within 48 h after the treatment. A change in urinary aspartate aminotransferase (AST) activity after mercury treatment followed a pattern similar to that observed with the urinary NAG. BGD treatment did not increase the urinary excretions of gamma-GTP, NAG, and AST. The uptake of p-aminohippuric acid (PAH) by renal cortical slices significantly decreased 24 h after mercury treatment. BGD injection after mercury treatment did not decrease the uptake of PAH by cortical slices. In addition, the microscopic examination of renal tissue from mercury-treated rats revealed necrosis of the proximal tubular cells. However, a photomicrograph of rat renal cortex after BGD treatment showed little abnormality. These results indicated that the mercury-induced renal damage was protected by the injection of BGD 30 min after mercury treatment.

摘要

研究了N-苄基-D-葡糖胺二硫代氨基甲酸盐(BGD)对大鼠无机汞肾毒性的影响。大鼠静脉注射生理盐水或HgCl2(300微克汞/千克),30分钟后腹腔注射生理盐水或BGD(2778微摩尔/千克,半数致死量的四分之一)。与对照组相比,汞处理后大鼠尿中刷状缘酶γ-谷氨酰转肽酶(γ-GTP)的排泄量在12 - 24小时尿标本中显著增加,并在处理后24小时内达到最大值。溶酶体酶N-乙酰-β-D-氨基葡萄糖苷酶(NAG)的尿排泄量在汞处理后与对照组相比在12 - 24小时尿标本中也显著增加,并在处理后48小时内达到最大值。汞处理后尿中天冬氨酸转氨酶(AST)活性的变化模式与尿NAG相似。BGD处理未增加γ-GTP、NAG和AST的尿排泄量。汞处理24小时后肾皮质切片对对氨基马尿酸(PAH)的摄取显著降低。汞处理后注射BGD未降低皮质切片对PAH的摄取。此外,对汞处理大鼠肾组织的显微镜检查显示近端肾小管细胞坏死。然而,BGD处理后大鼠肾皮质的显微照片显示几乎没有异常。这些结果表明,汞处理30分钟后注射BGD可保护汞诱导的肾损伤。

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