کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9035169 | 1132671 | 2005 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A comparison of hepatocyte cytotoxic mechanisms for chromate and arsenite
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کلمات کلیدی
BHAN,N′-Diphenyl-1,4-phenylenediamineDPPDBCNUdichlorofluoresceinMPTTBARSGSSGGSHTCAEGTADcfRPMHEPESBHT4-(2-hydroxyethyl)-1-piperazine-ethanesulfonic acid - 4- (2-hydroxyethyl) -1-piperazine-ethanesulfonic acidBSA - BSADMSO - DMSOROS - ROSarsenite - آرسنیتbovine serum albumin - آلبومین سرم گاوtrichloroacetic acid - اسید ترشکلراکتیکmitochondrial permeability transition - انتقال نفوذپذیری میتوکندریReduction - اکسایشbutylated hydroxy toluene - بوتیل هیدروکسی تولوئنanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of varianceOxidative stress - تنش اکسیداتیوstandard error - خطای استانداردstandard error of mean - خطای استاندارد میانگینDimethyl sulfoxide - دیمتیل سولفواکسیدSOD - سدCytotoxicity - سمیت سلولیSuperoxide dismutase - سوکسوکس دیسموتازLysosomes - لیزوزوم هاMethylation - متیلاسیونSEM - مدل معادلات ساختاری / میکروسکوپ الکترونی روبشیMitochondria - میتوکندریاHepatocyte - هپاتوسیتbutylated hydroxyanisole - هیدروکسی آنیزول باتلاقیrotations per minute - چرخش در دقیقهChromate - کروماتglutathione (oxidized form) - گلوتاتیون (فرم اکسید شده)glutathione (reduced form) - گلوتاتیون (فرم کاهش یافته)Reactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: A comparison of hepatocyte cytotoxic mechanisms for chromate and arsenite A comparison of hepatocyte cytotoxic mechanisms for chromate and arsenite](/preview/png/9035169.png)
چکیده انگلیسی
In the following, we have compared the cytotoxic mechanisms of the chromate CrO42â and arsenite AsO2â. Chromate (Cr (VI)) cytotoxicity was associated with reactive oxygen species (ROS) formation, lipid peroxidation and loss of mitochondrial membrane potential, which were prevented by catalase, antioxidants and ROS scavengers. Hepatocyte glutathione was also rapidly oxidized. Chromate reduction was inhibited in glutathione depleted hepatocytes, and glutathione depleted hepatocytes were also much more resistant to chromate induced cytotoxicity, ROS formation and lipid peroxidation. This suggests that chromate is reductively activated by glutathione. Chromate cytotoxicity also involved lysosomal injury and protease activation, which were prevented by lysosomotropic agents, endocytosis inhibitors, protease inhibitors and ROS scavengers. On the other hand, arsenite cytotoxicity was associated with much less oxidative stress, and lysosomal damage did not occur. However, arsenite cytotoxicity was also associated with loss of mitochondrial membrane potential, which in contrast to chromate cytotoxicity was inhibited by the ATP generators fructose, xylitol and glutamine. Arsenite induced cytotoxicity, mitochondrial membrane potential decline and also ROS formation were significantly increased by inactivating hepatocyte methionine synthase or hepatocyte methyl transferase. However, methyl donors such as betaine, methionine or folic acid prevented arsenite but not chromate cytotoxicity, and this suggests that arsenite is detoxified by reductive methylation. In conclusion, chromate induced cytotoxicity could be attributed to oxidative stress and lysosomal damage, whereas arsenite induced cytotoxicity could be attributed to mitochondrial toxicity and ATP depletion.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology - Volume 206, Issue 3, 31 January 2005, Pages 449-460
Journal: Toxicology - Volume 206, Issue 3, 31 January 2005, Pages 449-460
نویسندگان
Jalal Pourahmad, Maryam Rabiei, Farzaneh Jokar, Peter J. O'Brien,