pdc诱导睾丸毒性的机制：氧化应激、类固醇抑制和ZnO-NP/TEO协同作用的调节

IF 3.5 3区医学 Q2 FOOD SCIENCE & TECHNOLOGY

Food and Chemical Toxicology Pub Date : 2025-07-31 DOI:10.1016/j.fct.2025.115675

Asmaa S. Morsi , Hager M. Ramadan , Ahmed M. Youssef , Nadia A. Taha

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引用次数: 0

摘要

重铬酸钾（PDC）是一种强效的工业毒物，可引起严重的睾丸损伤，但其确切机制尚未完全确定。本研究探讨了雄性Sprague-Dawley大鼠（n = 108） pdcs诱导生殖毒性的机制途径。将大鼠分为9组：对照组（口服、腹腔注射）(I)、（II）、纯PDC （10.5 mg/kg bwt， III）、氧化锌纳米颗粒，纯ZnO-NPs （5 mg/kg bwt， IV）、百里香精油，纯TEO （5 mg/kg bwt， V）、ZnO-NPs + TEO （VI）、PDC + ZnO-NPs （VII）、PDC + TEO （VIII）和PDC + ZnO-NPs + TEO (IX)，治疗8周。PDC暴露引发了显著的睾丸氧化应激，丙二醛（MDA）和一氧化氮（Nox）活性升高，过氧化氢酶、谷胱甘肽和总抗氧化剂均减少。这种氧化还原失衡与精子生成和甾体生成受损直接相关，表现为睾丸重量减少，血清游离睾酮、LH和FSH水平降低，精子质量（活力、数量、形态）受损，以及甾体生成基因（StAR、CYP11A1、HSD-3β）下调。组织病理学分析证实精管变性和生殖细胞凋亡。关键是，抗氧化剂(TEO, ZnO-NPs；单独/联合)证实氧化应激和类固醇原性破坏是PDC睾丸毒性的主要驱动因素。这些发现明确了pdc诱导生殖损伤的机制基础，强调了其对氧化还原平衡和内分泌功能的破坏。

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Mechanisms of PDC-induced testicular Toxicity: Oxidative stress, steroidogenic suppression, and modulation by ZnO-NP/TEO synergy

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Mechanisms of PDC-induced testicular Toxicity: Oxidative stress, steroidogenic suppression, and modulation by ZnO-NP/TEO synergy

Potassium dichromate (PDC), a potent industrial toxicant, induces severe testicular damage, though its precise mechanisms remain incompletely defined. This study investigated the mechanistic pathways of PDC-induced reproductive toxicity in male Sprague-Dawley rats (n = 108). Rats were allocated into 9 groups: controls (oral, intraperitoneal) (I),(II), PDC-only (10.5 mg/kg bwt, III), Zinc Oxide Nanoparticles, ZnO-NPs-only (5 mg/kg bwt, IV), Thyme Essential Oil, TEO-only (5 mg/kg bwt, V), ZnO-NPs + TEO (VI), PDC + ZnO-NPs (VII), PDC + TEO (VIII), and PDC + ZnO-NPs + TEO (IX), treated for 8 weeks. PDC exposure triggered significant testicular oxidative stress, evidenced by elevated malondialdehyde (MDA) and Nitric oxide (Nox) activity alongside depleted catalase, glutathione, and total antioxidants. This redox imbalance directly correlated with impaired spermatogenesis and steroidogenesis, manifesting as reduced testis weight, decreased serum free testosterone, LH, and FSH levels, compromised sperm quality (motility, count, morphology), and downregulation steroidogenic genes (StAR, CYP11A1, HSD-3β). Histopathological analysis confirmed seminiferous tubule degeneration and germ cell apoptosis. Critically, reversal of these effects by antioxidants (TEO, ZnO-NPs; alone/combined) validated oxidative stress and steroidogenic disruption as primary drivers of PDC testicular toxicity. These findings define the mechanistic basis of PDC-induced reproductive injury, highlighting its disruption of redox balance and endocrine function.

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来源期刊

Food and Chemical Toxicology 工程技术-毒理学

CiteScore

10.90

自引率

4.70%

发文量

651

审稿时长

31 days

期刊介绍： Food and Chemical Toxicology (FCT), an internationally renowned journal, that publishes original research articles and reviews on toxic effects, in animals and humans, of natural or synthetic chemicals occurring in the human environment with particular emphasis on food, drugs, and chemicals, including agricultural and industrial safety, and consumer product safety. Areas such as safety evaluation of novel foods and ingredients, biotechnologically-derived products, and nanomaterials are included in the scope of the journal. FCT also encourages submission of papers on inter-relationships between nutrition and toxicology and on in vitro techniques, particularly those fostering the 3 Rs. The principal aim of the journal is to publish high impact, scholarly work and to serve as a multidisciplinary forum for research in toxicology. Papers submitted will be judged on the basis of scientific originality and contribution to the field, quality and subject matter. Studies should address at least one of the following: -Adverse physiological/biochemical, or pathological changes induced by specific defined substances -New techniques for assessing potential toxicity, including molecular biology -Mechanisms underlying toxic phenomena -Toxicological examinations of specific chemicals or consumer products, both those showing adverse effects and those demonstrating safety, that meet current standards of scientific acceptability. Authors must clearly and briefly identify what novel toxic effect (s) or toxic mechanism (s) of the chemical are being reported and what their significance is in the abstract. Furthermore, sufficient doses should be included in order to provide information on NOAEL/LOAEL values.