Meng Xiaojia, Li Li, An Hongmei, Deng Yaxin, Ling Chunmei, Lu Tianjiao, Song Guanling, Wang Yan
School of Medicine, Shihezi University, Shihezi, 832002, Xinjiang, China.
Biol Trace Elem Res. 2022 Jun;200(6):2825-2837. doi: 10.1007/s12011-021-02881-1. Epub 2021 Aug 16.
The research was carried out to investigate the possible ameliorative effect of lycopene on TiO NPs-induced male reproductive toxicity and explore the possible mechanism.
Ninety-six healthy male Institute of Cancer Research (ICR) mice were equally divided into eight groups (control group, 50 mg/kg TiO NPs group, 5 mg/kg LYC group, 20 mg/kg LYC group, 40 mg/kg LYC group, 50 mg/kg TiO NPs + 5 mg/kg LYC group, 50 mg/kg TiO NPs + 20 mg/kg LYC group, 50 mg/kg TiO NPs + 40 mg/kg LYC group), and the mice were treated by intragastric administration every day for 30 days in this research. Sperm parameters, testicular histopathology, oxidant and antioxidant enzymes, and cell apoptosis-related protein expression in the testicular tissue were analyzed.
The results showed that TiO NPs exposure significantly decreased sperm count and motility, and TiO NPs also increased sperm malformation in the epididymis; these characteristics were improved when co-administration with LYC. Testicular histopathological lesions like disorder of germ cells arrange, detachment, atrophy, and vacuolization were observed after TiO NPs exposure, and these abnormalities were effectively ameliorated by co-administration with LYC. Oxidative stress was induced by TiO NPs exposure as evidenced by increased the level of MDA and decreased the activity of SOD as well as the level of anti-O, and these alterations were effectively prevented by co-administration with LYC. LYC also alleviated TiO NPs-induced germ cell apoptosis by inhibiting mitochondrial apoptotic pathway, as shown by the upregulation of Bcl-2, the downregulation of Bax, Cleaved Caspase 3, and Cleaved Caspase 9.
LYC could ameliorate TiO NPs-induced testicular damage via inhibiting oxidative stress and apoptosis, which could be used to alleviate the testicular toxicity associated with TiO NPs intake.
本研究旨在探讨番茄红素对二氧化钛纳米颗粒诱导的雄性生殖毒性的可能改善作用,并探索其可能机制。
将96只健康的雄性癌症研究所(ICR)小鼠平均分为八组(对照组、50mg/kg二氧化钛纳米颗粒组、5mg/kg番茄红素组、20mg/kg番茄红素组、40mg/kg番茄红素组、50mg/kg二氧化钛纳米颗粒+5mg/kg番茄红素组、50mg/kg二氧化钛纳米颗粒+20mg/kg番茄红素组、50mg/kg二氧化钛纳米颗粒+40mg/kg番茄红素组),本研究中每天对小鼠进行灌胃给药,持续30天。分析精子参数、睾丸组织病理学、氧化和抗氧化酶以及睾丸组织中细胞凋亡相关蛋白表达。
结果表明,暴露于二氧化钛纳米颗粒会显著降低精子数量和活力,二氧化钛纳米颗粒还会增加附睾中精子的畸形率;与番茄红素共同给药时,这些特征得到改善。暴露于二氧化钛纳米颗粒后观察到睾丸组织病理学病变,如生殖细胞排列紊乱、脱落、萎缩和空泡化,与番茄红素共同给药可有效改善这些异常。二氧化钛纳米颗粒暴露诱导了氧化应激,表现为丙二醛水平升高、超氧化物歧化酶活性降低以及抗O水平降低,与番茄红素共同给药可有效预防这些变化。番茄红素还通过抑制线粒体凋亡途径减轻了二氧化钛纳米颗粒诱导的生殖细胞凋亡,表现为Bcl-2上调、Bax、裂解的半胱天冬酶3和裂解的半胱天冬酶9下调。
番茄红素可通过抑制氧化应激和细胞凋亡来改善二氧化钛纳米颗粒诱导的睾丸损伤,可用于减轻与摄入二氧化钛纳米颗粒相关的睾丸毒性。