کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8423048 | 1545967 | 2018 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A critical role for very long-chain fatty acid elongases in oleic acid-mediated Saccharomyces cerevisiae cytotoxicity
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کلمات کلیدی
MDAMethane dicarboxylic aldehydeCATTBARSVLCFAUFAGSHNACGPXROS - ROSAscorbic acid - آسکوربیک اسیدOleic acid - اسید اولئیکFatty acid - اسید چربVery long chain fatty acid - اسید چرب زنجیره ای بسیار طولانیPolyunsaturated fatty acid - اسید چرب غیر اشباعunsaturated fatty acid - اسید چرب غیر اشباعPUFA - اسید چرب چند غیراشباعvery long-chain fatty acids - اسیدهای چرب بسیار زنجیره ایOxidative stress - تنش اکسیداتیوSOD - سدLipotoxicity - سمیت لیپتوSuperoxide dismutase - سوکسوکس دیسموتازthiobarbituric acid reactive substances - مواد واکنش پذیر اسید تیوباربیتوریکMembrane permeability - نفوذپذیری غشاءN-acetyl cysteine - نیتستیل سیستئینOLA - همه چیزCatalase - کاتالازGlutathione - گلوتاتیونglutathione peroxidase - گلوتاتیون پراکسیدازReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیوتکنولوژی یا زیستفناوری
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Elongases FEN1/ELO2 and SUR4/ELO3 are important enzymes involved in the elongation of long-chain fatty acids (LCFAs) to very long-chain fatty acids (VLCFAs) in Saccharomyces cerevisiae. The molecular mechanism of the involvement of these elongases in lipotoxicity is unclear. In the present study, we investigated the role of VLCFA elongases in oleic acid-mediated yeast cytotoxicity. The spot test showed that yeast strains with the deletion of ELO2 or ELO3 were strikingly sensitive to oleic acid, while there was no change on the growth of strain with deleted ELO1 which was involved in the elongation of C14 fatty acid (FA) to C16 FA. By using GC-MS, the unsaturation index was increased in elo2â³ and elo3â³ mutants after treatment with oleic acid (OLA). However, the proportion of VLCFAs was increased in response to OLA in the wild-type strain. The growth inhibition of elo2â³ and elo3â³ could be partially rescued by two commonly used antioxidant agents N-acetyl cysteine (NAC) and Ascorbic acid (VC). The further study showed that exposure to excess OLA led to an increase in the levels of reactive oxygen species (ROS) and thiobarbituric acid reactive substances (TBARS), and a decline in the quantity of reduced glutathione (GSH) in both the wild type and mutant strains. However, the antioxidant enzyme activities of superoxide dismutase (SOD) and catalase (CAT) were increased in the wild type and elo1â³ strains, while they were significantly decreased in the mutants of elo2â³ and elo3â³ after treated with excess OLA. Thus, oxidative damage mainly contributed to the cell death induced by OLA in ole2â³ and ole3â³. Taken together, although disruption of ELO2 or ELO3 did not affect the cellular lipid unsaturation, they altered the distribution and propotion of cellular VLCFAs, leading to the cell membrane impairment, which augmented the ability of OLA to permeabilize the plasma membrane. The data suggest that the very long-chain fatty acids elongases ELO2 and ELO3 play important roles in lipotoxic cell death induced by OLA through maintaining a balanced FA composition in plasma membrane.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Microbiological Research - Volume 207, March 2018, Pages 1-7
Journal: Microbiological Research - Volume 207, March 2018, Pages 1-7
نویسندگان
Qiao Wang, Xiuxiu Du, Ke Ma, Ping Shi, Wenbin Liu, Jing Sun, Min Peng, Zhiwei Huang,