Ottupurakkal Savina K, Jayadevi Variyar E, Ramkumar K M, Jayasuriya R
Department of Biotechnology and Microbiology, Kannur University, Kannur, Kerala 670661, India.
Department of Biotechnology, School of Bioengineering, SRM Institute of Science and Technology, Kattankulathur, Tamil Nadu 603 203, India.
Toxicol Rep. 2025 Mar 12;14:101988. doi: 10.1016/j.toxrep.2025.101988. eCollection 2025 Jun.
Methoxychlor (MXC), a widely used pesticide, poses significant toxicological risks to various biological systems. It is an environmental contaminant and the only organochlorine pesticide still using instead of DDT. Endocrine disruption of MXC is also under investigation.This study aimed to investigate the effects of MXC on antioxidant status, lipid peroxidation, and liver metabolism in experimental rats.
Male Wistar rats were divided into control and treatment groups, with the latter receiving 150 mg/kg and 250 mg/kg body weight (BW) of MXC via oral administration for 30 days. Liver function was assessed by measuring circulating biomarkers, including Alanine Transaminase (ALT), Aspartate Transaminase (AST), and Alkaline Phosphatase (ALP). Oxidative damage was evaluated by determining Thiobarbituric Acid Reactive Substances (TBARS), hydroperoxide (HYP), and other lipid peroxidation markers. Key enzymes involved in antioxidant defense mechanisms were also analyzed in the liver of experimental animals.
Our results demonstrated a significant increase in ALT, AST, and ALP levels in the serum of rats exposed to MXC, indicating impaired liver function. This was accompanied by elevated lipid peroxidation, further emphasizing oxidative stress. Moreover, the activities of antioxidant enzymes such as SOD, GPx, and CAT were markedly reduced in the MXC-exposed groups compared to the controls, suggesting a compromised antioxidant defense system.
These findings suggest that methoxychlor exposure disrupts liver function and induces oxidative stress by enhancing lipid peroxidation, thereby depleting natural antioxidant defenses. This study highlights the potential hepatotoxic effects of methoxychlor and underscores the role of oxidative stress in mediating its toxicity.
甲氧滴滴涕（MXC）是一种广泛使用的杀虫剂，对各种生物系统构成重大毒理学风险。它是一种环境污染物，也是唯一仍在使用而非滴滴涕的有机氯杀虫剂。MXC的内分泌干扰作用也在研究中。本研究旨在探讨MXC对实验大鼠抗氧化状态、脂质过氧化和肝脏代谢的影响。
将雄性Wistar大鼠分为对照组和治疗组，后者通过口服给予150mg/kg和250mg/kg体重（BW）的MXC，持续30天。通过测量循环生物标志物，包括丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）和碱性磷酸酶（ALP）来评估肝功能。通过测定硫代巴比妥酸反应物质（TBARS）、氢过氧化物（HYP）和其他脂质过氧化标志物来评估氧化损伤。还分析了实验动物肝脏中参与抗氧化防御机制的关键酶。
我们的结果表明，暴露于MXC的大鼠血清中ALT、AST和ALP水平显著升高，表明肝功能受损。这伴随着脂质过氧化的升高，进一步强调了氧化应激。此外，与对照组相比，暴露于MXC的组中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GPx）和过氧化氢酶（CAT）等抗氧化酶的活性明显降低，表明抗氧化防御系统受损。
这些发现表明，甲氧滴滴涕暴露会破坏肝功能，并通过增强脂质过氧化诱导氧化应激，从而耗尽天然抗氧化防御。本研究突出了甲氧滴滴涕的潜在肝毒性作用，并强调了氧化应激在介导其毒性中的作用。
