István Fodor , János Schmidt , Réka Svigruha , Zita László , László Molnár , Sándor Gonda , Károly Elekes , Zsolt Pirger
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引用次数: 0
Abstract
Over the last 20 years, tributyltin (TBT) has been reported to cause metabolic disruption in both invertebrates and vertebrates, highlighting the need for further detailed analysis of its physiological effects. This study aimed to investigate the metabolic-disrupting effects of TBT from the behavioral to the molecular level. Adult specimens of the great pond snail (Lymnaea stagnalis) were exposed to an environmentally relevant concentration (100 ng L-1) of TBT for 21 days. After the chronic exposure, behavioral alterations as well as histological, cellular, and molecular changes were investigated in the central nervous system, kidney, and hepatopancreas. TBT exposure significantly decreased feeding activity, while locomotor activity remained unchanged. At the histological level, the cellular localization of tin was demonstrated in all tissues investigated and, in addition, characteristic morphological changes were observed in the kidney and hepatopancreas. Tissue-specific changes in lipid profiles confirmed TBT-induced disruption of lipid homeostasis in mollusks, characterized by a consistent reduction in the proportion of polyunsaturated fatty acids and a shift toward more saturated lipids. The expression of 17β-hydroxysteroid dehydrogenase type 12 (HSD17B12) enzyme, involved in lipid metabolism in vertebrates, was reduced in all three tissues after TBT exposure. Our results show that TBT induces significant multi-level metabolic changes in Lymnaea, including direct alterations in feeding activity and lipid composition. Our findings also suggest that HSD17B12 enzyme plays a key role in lipid metabolism in mollusks, as in mammals, and is likely involved in TBT-induced metabolic disruption. Overall, our study extends the findings of previous studies on mollusks by providing novel behavioral as well as tissue-specific histological and metabolic data and highlights the complexity and evolutionary conserved way of TBT-induced metabolic disruption.
在过去的20年里,三丁基锡(TBT)已被报道在无脊椎动物和脊椎动物中引起代谢紊乱,强调需要进一步详细分析其生理作用。本研究旨在从行为水平到分子水平探讨TBT的代谢干扰作用。采用环境相关浓度(100 ng L-1)的TBT处理大塘螺(lynaea滞螺)成虫21 d。慢性暴露后,研究了中枢神经系统、肾脏和肝胰腺的行为改变以及组织学、细胞和分子变化。TBT暴露显著降低了摄食活动,而运动活动保持不变。在组织学水平上,锡在所有被研究的组织中都有细胞定位,此外,在肾和肝胰腺中观察到特征性的形态学变化。脂质谱的组织特异性变化证实了tbt诱导的软体动物脂质稳态破坏,其特征是多不饱和脂肪酸比例持续减少,向更饱和的脂质转变。参与脊椎动物脂质代谢的17β-羟基类固醇脱氢酶12型(HSD17B12)酶在TBT暴露后在所有三种组织中的表达均降低。我们的研究结果表明,TBT诱导了淋巴细胞显著的多层次代谢变化,包括摄食活性和脂质组成的直接改变。我们的研究结果还表明,HSD17B12酶在软体动物的脂质代谢中起着关键作用,就像在哺乳动物中一样,并且可能参与了tbt诱导的代谢中断。总的来说,我们的研究通过提供新的行为以及组织特异性的组织学和代谢数据,扩展了先前对软体动物的研究结果,并突出了tbt诱导的代谢破坏的复杂性和进化保守方式。
期刊介绍:
Aquatic Toxicology publishes significant contributions that increase the understanding of the impact of harmful substances (including natural and synthetic chemicals) on aquatic organisms and ecosystems.
Aquatic Toxicology considers both laboratory and field studies with a focus on marine/ freshwater environments. We strive to attract high quality original scientific papers, critical reviews and expert opinion papers in the following areas: Effects of harmful substances on molecular, cellular, sub-organismal, organismal, population, community, and ecosystem level; Toxic Mechanisms; Genetic disturbances, transgenerational effects, behavioral and adaptive responses; Impacts of harmful substances on structure, function of and services provided by aquatic ecosystems; Mixture toxicity assessment; Statistical approaches to predict exposure to and hazards of contaminants
The journal also considers manuscripts in other areas, such as the development of innovative concepts, approaches, and methodologies, which promote the wider application of toxicological datasets to the protection of aquatic environments and inform ecological risk assessments and decision making by relevant authorities.