کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9018313 | 1128698 | 2005 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Hepatic mitochondrial glutathione: transport and role in disease and toxicity
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کلمات کلیدی
MMPTNFHMGCoARASMasemitochondrial GSHmGSHN-acetyl-p-aminophenolCYP2E1UCP2DISCUPRAPAPGSSGSAMNACGSHN-acetylcysteine - N-استیل سیستئینROS - ROSS-adenosyl-L-methionine - S-adenosyl-L-metionineALD - آدرنولکودیستروفیOxidant stress - استرس اکسیدانacidic sphingomyelinase - اسفنجومیلیناز اسیدیalcohol-induced liver disease - بیماری کبدی ناشی از الکلtumor necrosis factor-α - تومور نکروز عامل αFree radicals - رادیکال آزادmitochondrial electron transport chain - زنجیره حمل و نقل الکترون الکترونیک میتوکندریcytochrome P450 2E1 - سیتوکروم P450 2E1endoplasmic reticulum - شبکه آندوپلاسمی Mitochondrial membrane permeabilization - نفوذ پذیری غشای میتوکندریUnfolded protein response - پاسخ پروتئین آشکارLipid peroxidation - پراکسیداسیون لیپیدdeath-inducing signaling complex - پیچیدگی سیگنالینگ ناشی از مرگreduced glutathione - کاهش گلوتاتیونcholesterol - کلسترولoxidized glutathione - گلوتاتیون اکسید شدهReactive 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
چکیده انگلیسی
Synthesized in the cytosol of cells, a fraction of cytosolic glutathione (GSH) is then transported into the mitochondrial matrix where it reaches a high concentration and plays a critical role in defending mitochondria against oxidants and electrophiles. Evidence mainly from kidney and liver mitochondria indicated that the dicarboxylate and the 2-oxoglutarate carriers contribute to the transport of GSH across the mitochondrial inner membrane. However, differential features between kidney and liver mitochondrial GSH (mGSH) transport seem to suggest the existence of additional carriers the identity of which remains to be established. One of the characteristic features of the hepatic mitochondrial transport of GSH is its regulation by membrane fluidity. Conditions leading to increased cholesterol deposition in the mitochondrial inner membrane such as in alcohol-induced liver injury decrease membrane fluidity and impair the mitochondrial transport of GSH. Depletion of mitochondrial GSH by alcohol is believed to contribute to the sensitization of the liver to alcohol-induced injury through tumor necrosis factor (TNF)-mediated hepatocellular death. Through control of mitochondrial electron transport chain-generated oxidants, mitochondrial GSH modulates cell death and hence its regulation may be a key target to influence disease progression and drug-induced cell death.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology and Applied Pharmacology - Volume 204, Issue 3, 1 May 2005, Pages 263-273
Journal: Toxicology and Applied Pharmacology - Volume 204, Issue 3, 1 May 2005, Pages 263-273
نویسندگان
Jose C. Fernandez-Checa, Neil Kaplowitz,