Effect of cadmium on gap junctional intercellular communication in primary cultures of rat renal proximal tubular cells

被引：31

作者：

Fukumoto, M

Kujiraoka, T

Hara, M

Shibasaki, T

Hosoya, T

Yoshida, M

机构：

[1] St Marianna Univ, Sch Med, Dept Physiol, Miyamae Ku, Kawasaki, Kanagawa 2168511, Japan

[2] Jikei Univ, Sch Med, Dept Internal Med 2, Minato Ku, Tokyo 1058461, Japan

[3] St Marianna Univ, Sch Med, Dept Anat, Miyamae Ku, Kawasaki, Kanagawa 2168511, Japan

[4] Kyoritsu Coll Pharmaceut Sci, Dept Pharmaceut Therapeut, Minato Ku, Tokyo 1058512, Japan

[5] St Marianna Univ, Sch Med, Dept Chem, Miyamae Ku, Kawasaki, Kanagawa 2168511, Japan

来源：

LIFE SCIENCES | 2001年 / 69卷 / 03期

关键词：

cadmium; gap junction; primary culture; proximal tubular cells; rat; cytotoxicity; calcium; nitric oxide;

D O I：

10.1016/S0024-3205(01)01063-3

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Cadmium mainly accumulates in the kidney and causes renal injury. To clarify the mechanism of Cd nephrotoxicity, we investigated the effects of this element on intercellular communication through gap junction channels in primary cultures of rat renal proximal tubular cells. Sixty minutes after exposure to 100 muM Cd, dye coupling experiments showed that gap junctional intercellular communication (GJIC) was significantly inhibited. This inhibition occurred before the appearance of cytotoxicity. Intracellular calcium concentrations [Ca2+](i), which modulate the function of gap junctions, gradually increased after exposure to Cd and reached a maximum after 60 minutes. These results suggest that the inhibition of GJIC as a result of Cd exposure is related to an increase in [Ca2+](i). and that GJIC inhibition may be an indicator of nephrotoxicity, (C) 2001 Elsevier Science Inc. All rights reserved.

引用

页码：247 / 254

页数：8

共 29 条

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