<P> Cis-dichlorodiammine platinum II (Cisplatin), an effective chemotherapeutic agent, induces acute renal failure by unknown mechanisms. To investigate direct toxic effects of cisplatin on the renal proximal tubular transport system, LLC-PK<...
http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
https://www.riss.kr/link?id=A105379667
1997
-
518
SCIE,SCOPUS,KCI등재
학술저널
35-43(9쪽)
0
상세조회0
다운로드다국어 초록 (Multilingual Abstract)
<P> Cis-dichlorodiammine platinum II (Cisplatin), an effective chemotherapeutic agent, induces acute renal failure by unknown mechanisms. To investigate direct toxic effects of cisplatin on the renal proximal tubular transport system, LLC-PK<...
<P> Cis-dichlorodiammine platinum II (Cisplatin), an effective chemotherapeutic agent, induces acute renal failure by unknown mechanisms. To investigate direct toxic effects of cisplatin on the renal proximal tubular transport system, LLC-PK<SUB>1 </SUB>cell line was selected as a cell model and the sugar transport activity was evaluated during a course of cisplatin treatment. Cells grown to confluence were treated with cisplatin for 60 min, washed, and then incubated for up to 5 days. At appropriate intervals, cells were tested for sugar transport activity using α-methyl-D-[<SUP>14</SUP>C]glucopyranoside (AMG) as a model substrate. In cells treated with 100 ㄍM cisplatin, the AMG uptake was progressively impaired after 3 days. The viability of cells was not substantially changed with cisplatin of less than 100 ㄍM, but it decreased markedly with 150 and 200 ㄍM. In cisplatin-treated cells, the Na<SUP>+</SUP>-dependent AMG uptake was drastically inhibited with no change in the Na<SUP>+</SUP>-independent uptake. Kinetic analysis indicated that Vmax was suppressed, but Km was not altered. The Na<SUP>+</SUP>-dependent phlorizin binding was also decreased in cisplatin-treated cells. However, the AMG efflux from preloaded cells was not apparently retarded by cisplatin treatment. These data indicate that the cisplatin treatment impairs Na<SUP>+</SUP>-hexose cotransporters in LLC-PK<SUB>1</SUB> cells and suggest strongly that defects in transporter function at the luminal plasma membrane of the proximal tubular cells constitute an important pathogenic mechanism of cisplatin nephrotoxicity.
The Role of Adenosine Receptors on Acetylcholine Release in the Rat Striatum
Regulation of Adenosine Receptors in Rat Brain following Chronic Carbamazepine Treatment