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DBpiaThis study was designed to elucidate the mechanism of nephrotoxicity caused by antitumor agent tetraphosphine platinum (Ⅱ) complex (RC-1), which was synthesized as a tetraphosphine Pt (Ⅱ) derivatives recently. Rats treated with RC-1(20mg/kg/day) ...
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RISS 인기검색어
항암성 백금화합물의 신장독성에 관한 연구 = Studies on the Mechanism of Nephrotoxicity Caused by Antitumor Platinum Complex
한글로보기https://www.riss.kr/link?id=A45023256
- 저자
- 발행기관
- 학술지명
- 권호사항
-
발행연도
1993
-
작성언어
Korean
-
KDC
539.905
-
등재정보
SCOPUS,KCI등재
-
자료형태
학술저널
- 발행기관 URL
-
수록면
23-32(10쪽)
- 제공처
-
0
상세조회 -
0
다운로드
부가정보
다국어 초록 (Multilingual Abstract)
This study was designed to elucidate the mechanism of nephrotoxicity caused by antitumor agent tetraphosphine platinum (Ⅱ) complex (RC-1), which was synthesized as a tetraphosphine Pt (Ⅱ) derivatives recently.
Rats treated with RC-1(20mg/kg/day) showed the increase of BUN value and malondialdehyde contents in kidney homogenate, compared to the control and which means the lipid peroxidation was a main cause of nephrotoxicity.
In order to investigate the cytotoxic mechanism of RC-1, we also tested and revealed the generation of oxygen free radicals derived from neutrophil stimulated by RC-1 and interaction of the oxygen free radicals with the erythrocyte membrane.
From the above results, we suggest that nephrotoxicity of general platinum (Ⅱ) antitumor compounds as well as RC-1 were inhibited by radical scavengers.
Rats treated with RC-1(20mg/kg/day) showed the increase of BUN value and malondialdehyde contents in kidney homogenate, compared to the control and which means the lipid peroxidation was a main cause of nephrotoxicity.
In order to investigate the cytotoxic mechanism of RC-1, we also tested and revealed the generation of oxygen free radicals derived from neutrophil stimulated by RC-1 and interaction of the oxygen free radicals with the erythrocyte membrane.
From the above results, we suggest that nephrotoxicity of general platinum (Ⅱ) antitumor compounds as well as RC-1 were inhibited by radical scavengers.
This study was designed to elucidate the mechanism of nephrotoxicity caused by antitumor agent tetraphosphine platinum (Ⅱ) complex (RC-1), which was synthesized as a tetraphosphine Pt (Ⅱ) derivatives recently.
Rats treated with RC-1(20mg/kg/day) showed the increase of BUN value and malondialdehyde contents in kidney homogenate, compared to the control and which means the lipid peroxidation was a main cause of nephrotoxicity.
In order to investigate the cytotoxic mechanism of RC-1, we also tested and revealed the generation of oxygen free radicals derived from neutrophil stimulated by RC-1 and interaction of the oxygen free radicals with the erythrocyte membrane.
From the above results, we suggest that nephrotoxicity of general platinum (Ⅱ) antitumor compounds as well as RC-1 were inhibited by radical scavengers.
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