关键词: Acrylamide Bcl-2-like protein 4 (Bax)/B-cell lymphoma 2 (Bcl2) apoptotic markers endocrine disruptor redox imbalance testicular injury testicular toxicity zinc

Mesh : Animals Male Rats Acrylamide / toxicity Antioxidants / pharmacology metabolism Apoptosis / drug effects bcl-2-Associated X Protein / metabolism pharmacology Heme Oxygenase-1 / metabolism pharmacology NF-E2-Related Factor 2 / metabolism NF-kappa B / metabolism Oxidative Stress / drug effects Proto-Oncogene Proteins c-bcl-2 / metabolism pharmacology Rats, Wistar Semen / metabolism Signal Transduction / drug effects Zinc / pharmacology

来  源:   DOI:10.1080/13510002.2024.2341537   PDF(Pubmed)

Abstract:
UNASSIGNED: Acrylamide is a toxic substance formed in some foods that require high-temperature cooking processes and has been implicated as a gonadotoxic agent. Zinc, on the other hand, is a known antioxidant with fertility-enhancing properties. Hence, this study was designed to explore the possible ameliorative effect of zinc in acrylamide-induced gonadotoxicity.
UNASSIGNED: Twenty-four male Wistar rats were randomized into control, acrylamide (10 mg/kg of acrylamide), acrylamide + 1 mg/kg of zinc, and acrylamide + 3 mg/kg of zinc. The administration was via the oral route and lasted for 56 days.
UNASSIGNED: Zinc treatment ameliorated acrylamide-impaired sperm quality, normal testicular histoarchitecture, and hormonal balance, which was accompanied by increased testicular malondialdehyde and interleukin-1β and decreased testicular superoxide dismutase (SOD) and catalase (CAT). Furthermore, zinc prevented acrylamide-induced downregulation of testicular nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and B-cell lymphoma 2 (BCl2) expression and upregulation of testicular nuclear factor kappa B (NF-κB) and bcl-2-like protein 4 (bax) expression.
UNASSIGNED: In conclusion, zinc may protect against acrylamide-induced testicular toxicity, mediated by its antioxidant, anti-inflammatory, and antiapoptotic effects.
摘要:
丙烯酰胺是在某些需要高温烹饪过程的食品中形成的有毒物质,并被认为是促性腺激素剂。锌,另一方面,是一种已知的抗氧化剂,具有增强生育力的特性。因此,本研究旨在探讨锌对丙烯酰胺诱导的性腺毒性的可能改善作用。
将24只雄性Wistar大鼠随机分为对照组,丙烯酰胺(10mg/kg丙烯酰胺),丙烯酰胺+1毫克/千克锌,和丙烯酰胺+3mg/kg锌。通过口服途径给药并持续56天。
锌治疗改善了丙烯酰胺受损的精子质量,正常的睾丸组织结构,荷尔蒙平衡,伴有睾丸丙二醛和白细胞介素-1β增加,睾丸超氧化物歧化酶(SOD)和过氧化氢酶(CAT)降低。此外,锌可防止丙烯酰胺诱导的睾丸核因子红细胞2相关因子2(Nrf2)的下调,血红素加氧酶-1(HO-1),和B细胞淋巴瘤2(BCl2)的表达和睾丸核因子κB(NF-κB)和bcl-2样蛋白4(bax)的表达上调。
总而言之,锌可以防止丙烯酰胺引起的睾丸毒性,由其抗氧化剂介导,抗炎,和抗凋亡作用。
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