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Elevated seasonal temperature disrupts prooxidant-antioxidant homeostasis and promotes cellular apoptosis in the American oyster, Crassostrea virginica, in the Gulf of Mexico: a field study
Cell Stress and Chaperones ( IF 3.8 ) Pub Date : 2021-09-15 , DOI: 10.1007/s12192-021-01232-2
Md Sadequr Rahman 1, 2 , Md Saydur Rahman 1, 3
Affiliation  

One of the major impacts of climate change has been the marked rise in global temperature. Recently, we demonstrated that high temperatures (1-week exposure) disrupt prooxidant-antioxidant homeostasis and promote cellular apoptosis in the American oyster. In this study, we evaluated the effects of seasonal sea surface temperature (SST) on tissue morphology, extrapallial fluid (EPF) conditions, heat shock protein-70 (HSP70), dinitrophenyl protein (DNP, an indicator of reactive oxygen species, ROS), 3-nitrotyrosine protein (NTP, an indicator of RNS), catalase (CAT), superoxide dismutase (SOD) protein expressions, and cellular apoptosis in gills and digestive glands of oysters collected on the southern Texas coast during the winter (15 °C), spring (24 °C), summer (30 °C), and fall (27 °C). Histological observations of both tissues showed a notable increase in mucus production and an enlargement of the digestive gland lumen with seasonal temperature rise, whereas biochemical analyses exhibited a significant decrease in EPF pH and protein concentration. Immunohistochemical analyses showed higher expression of HSP70 along with the expression of DNP and NTP in oyster tissues during summer. Intriguingly, CAT and SOD protein expressions exhibited significant upregulation with rising seasonal temperatures (15 to 27 °C), which decreased significantly in summer (30 °C), leaving oysters vulnerable to oxidative and nitrative damage. qRT-PCR analysis revealed a significant increase in HSP70 mRNA levels in oyster tissues during the warmer seasons. In situ TUNNEL assay showed a significant increase in apoptotic cells in seasons with high temperature. These results suggest that elevated SST induces oxidative/nitrative stress through the overproduction of ROS/RNS and disrupts the antioxidant system which promotes cellular apoptosis in oysters.



中文翻译:

季节性温度升高会破坏墨西哥湾美国牡蛎 Crassostrea virginica 的促氧化-抗氧化稳态并促进细胞凋亡:一项实地研究

气候变化的主要影响之一是全球气温显着上升。最近,我们证明高温(暴露 1 周)会破坏美国牡蛎的促氧化-抗氧化稳态并促进细胞凋亡。在这项研究中,我们评估了季节性海面温度 (SST) 对组织形态、外层液 (EPF) 条件、热休克蛋白 70 (HSP70)、二硝基苯基蛋白 (DNP,活性氧的指示剂,ROS) 的影响, 3-硝基酪氨酸蛋白 (NTP,RNS 的指标)、过氧化氢酶 (CAT)、超氧化物歧化酶 (SOD) 蛋白表达,以及在德克萨斯州南部海岸冬季(15 °C)采集的牡蛎鳃和消化腺的细胞凋亡)、春季 (24 °C)、夏季 (30 °C) 和秋季 (27 °C)。两种组织的组织学观察表明,随着季节性温度升高,粘液产生显着增加,消化腺管腔扩大,而生化分析显示 EPF pH 值和蛋白质浓度显着降低。免疫组织化学分析表明,夏季牡蛎组织中 HSP70 的表达较高,同时 DNP 和 NTP 的表达也较高。有趣的是,CAT 和 SOD 蛋白表达随着季节性温度升高(15 至 27°C)而显着上调,而在夏季(30°C)时显着降低,使牡蛎容易受到氧化和硝化损伤。qRT-PCR 分析显示,在温暖的季节,牡蛎组织中 HSP70 mRNA 水平显着增加。原位 TUNNEL 分析显示,在高温季节,凋亡细胞显着增加。这些结果表明,升高的 SST 通过过量产生 ROS/RNS 诱导氧化/硝化应激,并破坏促进牡蛎细胞凋亡的抗氧化系统。

更新日期:2021-09-16
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