Vocational School of Araban, University of Gaziantep, Araban-Gaziantep, Turkey.
Faculty of Medicine, Department of Histology and Embryology, University of Gaziantep, Gaziantep, Turkey.
Drug Chem Toxicol. 2022 Jul;45(4):1851-1861. doi: 10.1080/01480545.2021.1892128. Epub 2021 Mar 1.
This study was performed to investigate the tissue-specific effects of clothianidin on by evaluating the biochemical and histological alterations following 21 days of treatment to environmentally relevant concentrations of 3, 15, and 30 µg/L. The emerged behavioral changes in feeding and swimming performance were considered as adaptive responses to avoid the chemical. The toxic effect of pesticide on nervous system and osmoregulation was evidenced with the inhibition of AChE and NaK-ATPase. The sustained lipid peroxidation, ranging from muscle (196%) > brain (154%) > gill (140%) > kidney (129%), might be suggested as a mechanism mediating the inhibition of membrane-bound enzymes. Histological evaluation showed clothianidin-induced lesions appearing as necrosis, atrophy, and edema in muscle, hyperplasia, and hypertrophy causing shortening and fusion of the secondary lamellae in gill, vacuolization, and hydropic degeneration in brain, degeneration of tubular epithelium, and existence of melanomacrophage centers in kidney. The pronounced degenerative changes observed in gill indicate the vulnerability of tissue possibly due to its role as first contact and entry point for the pesticide. Consequently, clothianidin exerted its toxic effects by altering normal behavior, causing neurotoxicity and disturbing osmoregulation. Moreover, the imposed stress was responded in a tissue-specific manner and histological lesions become more severe with increasing concentration. The findings clearly reveal the potential threat caused by environmentally relevant concentrations of clothianidin to early life stages of fish.
本研究旨在通过评估在 21 天的治疗后，环境相关浓度为 3、15 和 30µg/L 的药剂对 组织的特异性影响，来研究噻虫嗪对 的影响。在接触化学物质时，出现的摄食和游泳行为改变被认为是一种适应性反应。农药对神经系统和渗透调节的毒性作用表现为乙酰胆碱酯酶和 NaK-ATP 酶的抑制。持续的脂质过氧化，范围从肌肉（196%）>大脑（154%）>鳃（140%）>肾脏（129%），可能被认为是一种介导膜结合酶抑制的机制。组织学评估显示，噻虫嗪引起的病变表现为肌肉坏死、萎缩和水肿，鳃的增生和肥大导致二级鳃片缩短和融合，脑的空泡化和水肿变性，肾小管上皮细胞变性，肾脏中存在黑色素巨噬细胞中心。在鳃中观察到的明显退行性变化表明，组织可能由于其作为农药的第一接触和进入点而变得脆弱。因此，噻虫嗪通过改变正常行为、引起神经毒性和扰乱渗透调节来发挥其毒性作用。此外，组织以特定的方式对施加的应激做出反应，并且随着浓度的增加，组织病变变得更加严重。这些发现清楚地揭示了环境相关浓度的噻虫嗪对鱼类早期生活阶段可能造成的潜在威胁。
