除草剂赛克对金鱼的肝毒性可能源于轻度氧化应激的诱导。
Hepatotoxicity of herbicide Sencor in goldfish may result from induction of mild oxidative stress.
作者信息
Maksymiv Ivan V, Husak Viktor V, Mosiichuk Nadia M, Matviishyn Tetiana M, Sluchyk Iryna Y, Storey Janet M, Storey Kenneth B, Lushchak Volodymyr I
机构信息
Department of Biochemistry and Biotechnology, Precarpathian National University named after Vasyl Stefanyk, 57 Shevchenko Str., Ivano-Frankivsk 76025, Ukraine.
Department of Human and Animal Anatomy and Physiology, Precarpathian National University named after Vasyl Stefanyk, 57 Shevchenko Str., Ivano-Frankivsk 76025, Ukraine.
出版信息
Pestic Biochem Physiol. 2015 Jul;122:67-75. doi: 10.1016/j.pestbp.2014.12.020. Epub 2014 Dec 22.
The effects of 96 h exposure to 7.14, 35.7, or 71.4 mg L(-1) of Sencor were studied on liver and plasma parameters in goldfish, Carassius auratus L. Goldfish exposure to 71.4 mg L(-1) of Sencor for 96 h resulted in a decrease in glucose concentrations in plasma and liver by 55%, but did not affect liver glycogen levels. An increase in the activity of aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase (by 24-27%, 32-72%, and 87-102%, respectively) occurred in plasma of Sencor exposed goldfish, whereas in liver activities of these enzymes decreased (by 15-17%, 19%, and 20%, respectively). Lactate concentration in plasma increased by 22-36% in all treated fish groups, whereas in liver it increased by 64% only after exposure to 35.7 mg L(-1) of Sencor. Herbicide exposure enhanced lipid peroxide levels by 49-75% and decreased activities of catalase by 46%, glutathione reductase by 25-48% and glutathione peroxidase by 21-26% suggesting development of oxidative stress in liver. The treatment induced various histological changes in goldfish liver, such as dilated sinusoids, hypertrophy and dystrophy of hepatic cells and detachment of endothelial cytoplasm with diffuse hemorrhage. The data collectively let us propose that mild oxidative stress might be responsible for the hepatotoxicity of Sencor.
研究了将金鱼（Carassius auratus L.）暴露于7.14、35.7或71.4 mg L⁻¹的甲磺隆96小时对其肝脏和血浆参数的影响。金鱼暴露于71.4 mg L⁻¹的甲磺隆中96小时后，血浆和肝脏中的葡萄糖浓度降低了55%，但未影响肝脏糖原水平。暴露于甲磺隆的金鱼血浆中天冬氨酸转氨酶、丙氨酸转氨酶和乳酸脱氢酶的活性增加（分别增加24 - 27%、32 - 72%和87 - 102%），而这些酶在肝脏中的活性降低（分别降低15 - 17%、19%和20%）。所有处理组的金鱼血浆中乳酸浓度增加了22 - 36%，而仅在暴露于35.7 mg L⁻¹的甲磺隆后，肝脏中的乳酸浓度增加了64%。除草剂暴露使脂质过氧化物水平提高了49 - 75%，过氧化氢酶活性降低了46%，谷胱甘肽还原酶活性降低了25 - 48%，谷胱甘肽过氧化物酶活性降低了21 - 26%，这表明肝脏中出现了氧化应激。该处理在金鱼肝脏中引起了各种组织学变化，如肝血窦扩张、肝细胞肥大和营养不良以及内皮细胞质脱离并伴有弥漫性出血。这些数据共同使我们提出，轻度氧化应激可能是甲磺隆肝毒性的原因。
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