Arsenic and polystyrene‐nano plastics co‐exposure induced testicular toxicity: Triggers oxidative stress and promotes apoptosis and inflammation in mice

氧化应激 毒性 细胞凋亡 化学 炎症 聚苯乙烯 砷毒性 纳米- 免疫学 生物化学 医学 材料科学 聚合物 复合材料 有机化学
作者
Gan Rao,Baoxin Qiao,Gaolong Zhong,Tong Li,Qian Su,Shaofeng Wu,Zhaoxin Tang,Lianmei Hu
出处
期刊:Environmental Toxicology [Wiley]
卷期号:39 (1): 264-276 被引量:17
标识
DOI:10.1002/tox.23970
摘要

Co-existing of polystyrene-nano plastics (PSNPs) and arsenic (As) in the environment caused a horrendous risk to human health. However, the potential mechanism of PSNPs and As combination induced testicular toxicity in mammals has not been elucidated. Therefore, we first explore the testicular toxicity and the potential mechanism in male Kunming mice exposed to As or/and PSNPs. Results revealed that compared to the As or PSNPs group, the combined group showed more significant testicular toxicity. Specifically, As and PSNPs combination induced irregular spermatozoa array and blood-testis barrier disruption. Simultaneously, As and PSNPs co-exposure also exacerbated oxidative stress, including increasing the MDA content, and down-regulating expression of Nrf-2, HO-1, SOD-1, and Trx. PSNPs and As combination also triggered testicular apoptosis, containing changes in apoptotic factors (P53, Bax, Bcl-2, Cytc, Caspase-8, Caspase-9, and Caspase-3). Furthermore, co-exposed to As and PSNPs aggravated inflammatory damage characterized by targeted phosphorylation of NF-κB and degradation of I-κB. In summary, our results strongly confirmed As + PSNPs co-exposure induced the synergistic toxicity of testis through excessive oxidative stress, apoptosis, and inflammation, which could offer a new sight into the mechanism of environmental pollutants co-exposure induced male reproductive toxicity.
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