Department of Physiological Sciences, Federal University of São Carlos, São Carlos, São Paulo, Brazil.
Department of Chemistry, Federal University of São Carlos, São Carlos, São Paulo, Brazil.
Environ Toxicol Chem. 2020 May;39(5):1041-1051. doi: 10.1002/etc.4696. Epub 2020 Mar 31.
Radiocystis fernandoi, a microcystin (MC) producer, has been common in cyanobacterial blooms in tropical regions. Microcystin is a hepatotoxin that causes tissue damage and even death in animals, including humans; its detoxification process may involve biotransformation and activation of the antioxidant defense system. We evaluated the detoxification pathway, examined the antioxidant defense system responses, and determined the alterations and the organ histopathological indexes in the liver of the tropical fish Hoplias malabaricus after acute and subchronic intraperitoneal exposure to microcystin. The crude microcystin extract of R. fernandoi had predominantly MC-RR and MC-YR. The detoxification process was activated by increasing ethoxyresorufin-O-deethylase activity, whereas glutathione S-transferase was inhibited. The activity of the antioxidant defense enzymes superoxide dismutase (SOD) and glutathione peroxidase decreased after acute exposure; the SOD-catalase system and the glutathione level increased after subchronic exposure. The carbonyl protein level, lipid peroxidation (LPO), and DNA damage were unchanged after acute exposure, whereas protein carbonyl was unchanged, LPO decreased, and DNA damage increased after subchronic exposure. Histopathological alteration indexes differed between acute and subchronic exposure, but the histopathological organ indexes indicate liver dysfunction in both exposure periods. We conclude that MC-RR and MC-YR induce different liver responses depending on the time of exposure, and the antioxidant defense responses after subchronic exposure may help to partially restore the liver function. Environ Toxicol Chem 2020;39:1041-1051. © 2020 SETAC.
费氏束丝藻是一种微囊藻毒素（MC）的生产者，在热带地区的蓝藻水华事件中很常见。MC 是一种肝毒素，会导致动物（包括人类）的组织损伤甚至死亡；其解毒过程可能涉及生物转化和抗氧化防御系统的激活。我们评估了热带鱼 Hoplias malabaricus 经急性和亚慢性腹腔内暴露于微囊藻毒素后的解毒途径，研究了抗氧化防御系统的反应，并确定了肝脏的变化和组织病理学指标。费氏束丝藻的粗微囊藻毒素提取物主要含有 MC-RR 和 MC-YR。解毒过程通过增加乙氧基试卤灵-O-去乙基酶的活性而被激活，而谷胱甘肽 S-转移酶则受到抑制。急性暴露后，抗氧化防御酶超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶的活性下降；亚慢性暴露后，SOD-过氧化氢酶系统和谷胱甘肽水平增加。急性暴露后，羰基蛋白水平、脂质过氧化（LPO）和 DNA 损伤没有变化，而亚慢性暴露后，蛋白质羰基没有变化，LPO 减少，DNA 损伤增加。急性和亚慢性暴露之间的组织病理学改变指标不同，但两个暴露期的组织病理学器官指标都表明肝脏功能障碍。我们得出结论，MC-RR 和 MC-YR 会根据暴露时间引起不同的肝脏反应，而亚慢性暴露后的抗氧化防御反应可能有助于部分恢复肝功能。环境毒理化学 2020；39：1041-1051。©2020 SETAC。
