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有机汞中毒对淡水鱼外周血及代谢物水平的影响

Effect of organomercurial poisoning on the peripheral blood and metabolite levels of a freshwater fish.

作者信息

Gill T S, Pant J C

出版信息

Ecotoxicol Environ Saf. 1985 Oct;10(2):150-8. doi: 10.1016/0147-6513(85)90061-2.

Abstract

This work evaluated the hematological and biochemical changes in the fish, Puntius conchonius, under experimental organomercurial poisoning. Long-term (8 weeks) exposure to 3.63 and 6.03 mg/liter methoxyethyl mercuric chloride (MEMC) (0.2 and 0.33 fractions of 96-hr LC50) led to morphological aberrations in mature erythrocytes including nuclear and cytoplasmic deterioration, vacuolation, chromatin condensation, and hypochromia. Immature erythrocytes showing membrane leakage were also encountered. Erythrocyte count and hemoglobin (Hb) were significantly lowered after 1 and 3 weeks followed by a marginal rise persisting upto 8 weeks. Differential leucocyte counts revealed significant thrombocytopenia, lymphocytosis, and neutropenia. Collateral evaluation of blood glucose and tissue glycogen levels revealed significant hyperglycemia as well as glycogen depletion in liver and brain. Heart glycogen content evinced a substantial increase after 5 and 8 weeks exposure.

摘要

本研究评估了实验性有机汞中毒情况下,玫瑰无须魮(Puntius conchonius)鱼的血液学和生化变化。长期(8周)暴露于3.63和6.03毫克/升的甲氧基乙基氯化汞(MEMC)(96小时半数致死浓度的0.2和0.33部分)会导致成熟红细胞出现形态畸变,包括细胞核和细胞质退化、空泡化、染色质凝聚和低色素性。还发现了显示膜泄漏的未成熟红细胞。红细胞计数和血红蛋白(Hb)在1周和3周后显著降低,随后略有上升并持续至8周。白细胞分类计数显示显著的血小板减少、淋巴细胞增多和中性粒细胞减少。对血糖和组织糖原水平的附带评估显示显著的高血糖以及肝脏和大脑中的糖原消耗。暴露5周和8周后,心脏糖原含量显著增加。

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