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首页> 外文期刊>Archives of Toxicology >Expression of Hsp70 in kidney cells exposed to ochratoxin A.
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Expression of Hsp70 in kidney cells exposed to ochratoxin A.

机译：Hsp70在暴露于och曲霉毒素A的肾细胞中的表达。

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Ochratoxin A (OTA) is a possible etiological agent of endemic nephropathy, a chronic renal disease with high prevalence in limited geographic areas. Ochratoxicosis has many characteristics of different pathological states in which heat shock proteins (Hsps) are usually induced. The most inducible heat shock proteins belong to the Hsp70 family. We determined the level of expression of Hsp70 by the Western blot analysis in kidneys of rats treated with low doses of OTA and in LLC-PK1 and MDCK cells exposed to OTA. Estimation of cell viability and release of lactate dehydrogenase (LDH) confirmed the toxic effects of OTA on cultured cells. OTA affects the relative distribution of two Hsp70 isoforms (68-kDa and 74-kDa isoforms), but does not change total amount of Hsp70 in rat kidney. No changes in the Hsp70 level were detected in LLC-PK1 and MDCK cells treated with OTA, although the cells were seriously injured, as was seen from the reduced cell viability and increased release of LDH. Both cell lines were capable of having Hsp70 induced following a heat shock. However, exposure of the cells to OTA before the heat shock challenge prevented Hsp70 induction. Results of the study show that OTA does not induce Hsp70 in rat kidney or in cultured kidney cells. The absence of Hsp70 protective effects in the cells and tissues might be a possible explanation for the cumulative destructive effects of OTA and a silent onset of endemic nephropathy in humans and of OTA-induced experimental nephrotoxicity in animals.
机译：ch曲霉毒素A（OTA）可能是地方性肾病的病原体，这是一种在有限的地理区域中患病率很高的慢性肾脏疾病。 ch曲中毒具有通常诱发热休克蛋白（Hsps）的不同病理状态的许多特征。最可诱导的热激蛋白属于Hsp70家族。我们通过蛋白质印迹分析确定了低剂量OTA处理的大鼠肾脏以及暴露于OTA的LLC-PK1和MDCK细胞中Hsp70的表达水平。估计细胞活力和释放乳酸脱氢酶（LDH）证实了OTA对培养细胞的毒性作用。 OTA影响两种Hsp70亚型（68-kDa和74-kDa亚型）的相对分布，但不会改变大鼠肾脏中Hsp70的总量。从OTA处理的LLC-PK1细胞和MDCK细胞中，虽然细胞受到了严重的损伤，但未检测到Hsp70水平的变化，这从细胞活力降低和LDH释放增加可见。两种细胞系均能够在热激后诱导Hsp70。但是，在热激攻击之前将细胞暴露于OTA阻止了Hsp70的诱导。研究结果表明，OTA不会在大鼠肾脏或培养的肾细胞中诱导Hsp70。细胞和组织中缺乏Hsp70保护作用可能是对OTA累积破坏作用和人类地方性肾病无声发作以及OTA引起的动物实验性肾毒性的可能解释。

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