The intensive applications of chlorpyrifos (CPF) in agricultural production have resulted in lethal effects on the environment, particularly on aquatic fauna. Thus, present study was aimed to assess the haematological responses, antioxidant enzymes (superoxide dismutase [SOD] and catalase [CAT]) activity, acetylcholinesterase enzyme (AChE) inhibition and histopathological alterations in liver and gill tissues of cold‐water fish rainbow trout (Oncorhynchus mykiss) in their native habitat, when exposed to CPF. In total, 240 fingerlings were subjected to various CPF concentrations (0, 2, 4 and 6 μg/L) for acute and sub‐lethal toxicity tests. Results revealed that increasing CPF concentration and exposure time have resulted in reduced erythrocyte count, haemoglobin concentration and haematocrit level; however, leucocyte count was increased. Additionally, decrease in AChE activity was also observed with increasing concentration. CPF concentrations at lowest exposure duration induced slight increase of SOD and CAT activity while the high exposure durations (14 and 21 days) exhausted the activity of antioxidant enzymes. Structural damages produced by CPF in liver tissues were hyperaemia, dilated central veins, sinusoids and degenerative changes, while the lesions observed in gill tissue were curling of secondary lamella, cell degeneration, cell necrosis, narrowing of water channels, hyperplasia, oedematous changes, fusion of secondary lamella and sloughing.

中文翻译：

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毒死蜱介导的巴基斯坦北部淡水鱼 Oncorhynchus mykiss 的氧化损伤和组织病理学改变

毒死蜱 (CPF) 在农业生产中的大量使用已对环境造成致命影响，尤其是对水生动物。因此，本研究旨在评估冷水鱼虹鳟鱼肝脏和鳃组织的血液学反应、抗氧化酶（超氧化物歧化酶 [SOD] 和过氧化氢酶 [CAT]）活性、乙酰胆碱酯酶（AChE）抑制和组织病理学改变。 Oncorhynchus mykiss) 在它们的原生栖息地，当暴露于 CPF 时。总共有 240 条鱼种接受了不同 CPF 浓度（0、2、4 和 6 μg/L）的急性和亚致死毒性测试。结果显示，增加 CPF 浓度和暴露时间导致红细胞计数、血红蛋白浓度和血细胞比容水平降低；然而，白细胞计数增加。此外，还观察到 AChE 活性随着浓度的增加而降低。CPF 浓度在最低暴露持续时间诱导 SOD 和 CAT 活性略有增加，而高暴露持续时间（14 天和 21 天）耗尽了抗氧化酶的活性。CPF在肝组织中产生的结构性损伤为充血、中央静脉扩张、血窦和退行性改变，而在鳃组织中观察到的损伤为次生薄层卷曲、细胞变性、细胞坏死、水道变窄、增生、水肿改变、融合次生薄片和脱落。CPF 浓度在最低暴露持续时间诱导 SOD 和 CAT 活性略有增加，而高暴露持续时间（14 天和 21 天）耗尽了抗氧化酶的活性。CPF在肝组织中产生的结构性损伤为充血、中央静脉扩张、血窦和退行性改变，而在鳃组织中观察到的损伤为次生薄层卷曲、细胞变性、细胞坏死、水道变窄、增生、水肿改变、融合次生薄片和脱落。CPF 浓度在最低暴露持续时间诱导 SOD 和 CAT 活性略有增加，而高暴露持续时间（14 天和 21 天）耗尽了抗氧化酶的活性。CPF在肝组织中产生的结构性损伤为充血、中央静脉扩张、血窦和退行性改变，而在鳃组织中观察到的损伤为次生薄层卷曲、细胞变性、细胞坏死、水道变窄、增生、水肿改变、融合次生薄片和脱落。