由于世界各地都使用消毒剂来治疗人类和其他动物的疾病,它们对人类健康构成重大风险。消毒剂对鱼肝的综合作用,尤其是对氧化应激的影响,毒理学效应,转录组概况,和细胞凋亡,尚未完全分析。在目前的调查中,健康草鱼暴露于80μg/L戊二醛或50μg/L聚维酮碘30天。首先,酶活性测试的结果表明,戊二醛的给药可以通过降低T-SOD来显著增加氧化应激,CAT,和GPx并提高MDA。此外,KEGG研究表明,暴露于戊二醛和聚维酮碘刺激了PPAR信号通路。为了进一步阐明转录组结果,验证了PPAR信号通路中相关DEGs的相对表达。戊二醛诱导草鱼肝组织凋亡;当暴露于戊二醛或聚维酮碘时,它激活了草鱼肝细胞的细胞毒性和凋亡。根据目前的研究,消毒剂会导致免疫系统受损,氧化应激,草鱼肝脏中PPAR信号通路的衰减,使它们作为草鱼的膳食补充剂有害,特别是在水产养殖领域。
Since disinfectants are used all over the world to treat illnesses in people and other animals, they pose a major risk to human health. The comprehensive effects of disinfectant treatments on fish liver, especially the impacts on oxidative stress, toxicological effects, transcriptome profiles, and apoptosis, have not yet been fully analyzed. In the current investigation, healthy grass carp were exposed to 80 μg/L
glutaraldehyde or 50 μg/L povidone-iodine for 30 days. First, the findings of enzyme activity tests demonstrated that the administration of
glutaraldehyde could considerably increase oxidative stress by lowering T-SOD, CAT, and GPx and raising MDA. Furthermore, KEGG research revealed that exposure to
glutaraldehyde and povidone-iodine stimulated the PPAR signal pathway. To further elucidate the transcriptome results, the relative expressions of related DEGs in the PPAR signal pathway were verified.
Glutaraldehyde induced apoptosis in liver tissue of grass carp; however, it activated cytotoxicity and apoptosis in grass carp hepatocytes when exposed to
glutaraldehyde or povidone-iodine. According to the current study, disinfectants can cause the impairment of the immune system, oxidative stress, and attenuation of the PPAR signal pathway in the liver of grass carp, making them detrimental as dietary supplements for grass carp, particularly in the aquaculture sector.