Concentration-dependent biphasic toxicity and steroidogenic stimulation by aminocarb in murine Leydig cells

IF 4.2 3区环境科学与生态学 Q2 ENVIRONMENTAL SCIENCES

Environmental toxicology and pharmacology Pub Date : 2025-07-30 DOI:10.1016/j.etap.2025.104777

Sílvia Moreira , Ana D. Martins , Raquel L. Bernardino , Marisa Pinho , Inês M.S. Guerra , M. Rosário Domingues , Marco G. Alves , Luis Miguel Pastor , Vicente Seco-Rovira , Maria de Lourdes Pereira , Pedro F. Oliveira

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Abstract

Exposure to environmental chemicals, like pesticides, can impair male reproductive health by affecting Leydig cell (LC) function. This study investigated aminocarb, a widely used carbamate pesticide, and its impact on murine LCs (BLTK1 cell line). We observed a concentration-dependent biphasic toxicity, where higher aminocarb concentrations (500 μM) reduced LC viability, while lower doses (5 and 50 μM) unexpectedly increased it. Aminocarb selectively disrupted mitochondrial complexes I and III without altering overall mitochondrial respiration or reactive oxygen species (ROS) production. Notably, 50 μM aminocarb enhanced androstenedione production, a key androgen precursor. This research highlights the nuanced impact of aminocarb on LCs, suggesting targeted mitochondrial effects and steroidogenic stimulation, with implications for male reproductive health and environmental toxicology.

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氨基威对小鼠间质细胞的浓度依赖性双相毒性和甾体性刺激。

暴露于环境中的化学物质，如杀虫剂，可以通过影响间质细胞（LC）的功能来损害男性生殖健康。本研究研究了氨基甲酸酯类农药氨基威（aminocarb）对小鼠LCs （BLTK1细胞系）的影响。我们观察到浓度依赖的双相毒性，较高的氨基威浓度（500μM）降低了LC活力，而较低的剂量（5和50μM）意外地增加了LC活力。氨基威选择性地破坏线粒体复合体I和III，而不改变线粒体呼吸或活性氧（ROS）的产生。值得注意的是，50μM aminocarb增强了雄烯二酮的生成，雄烯二酮是一种关键的雄激素前体。这项研究强调了氨基威对LCs的细微影响，表明有针对性的线粒体效应和类固醇刺激，对男性生殖健康和环境毒理学有影响。

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来源期刊

Environmental toxicology and pharmacology 医学-毒理学

CiteScore

7.00

自引率

4.70%

发文量

185

审稿时长

34 days

期刊介绍： Environmental Toxicology and Pharmacology publishes the results of studies concerning toxic and pharmacological effects of (human and veterinary) drugs and of environmental contaminants in animals and man. Areas of special interest are: molecular mechanisms of toxicity, biotransformation and toxicokinetics (including toxicokinetic modelling), molecular, biochemical and physiological mechanisms explaining differences in sensitivity between species and individuals, the characterisation of pathophysiological models and mechanisms involved in the development of effects and the identification of biological markers that can be used to study exposure and effects in man and animals. In addition to full length papers, short communications, full-length reviews and mini-reviews, Environmental Toxicology and Pharmacology will publish in depth assessments of special problem areas. The latter publications may exceed the length of a full length paper three to fourfold. A basic requirement is that the assessments are made under the auspices of international groups of leading experts in the fields concerned. The information examined may either consist of data that were already published, or of new data that were obtained within the framework of collaborative research programmes. Provision is also made for the acceptance of minireviews on (classes of) compounds, toxicities or mechanisms, debating recent advances in rapidly developing fields that fall within the scope of the journal.