Arsenic and polystyrene-nano plastics co-exposure induced testicular toxicity: Triggers oxidative stress and promotes apoptosis and inflammation in mice.
Gan RaoBaoxin QiaoGaolong ZhongTong LiQian SuShaofeng WuZhaoxin TangLianmei HuPublished in: Environmental toxicology (2023)
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.
Keyphrases
- oxidative stress
- diabetic rats
- induced apoptosis
- ischemia reperfusion injury
- dna damage
- human health
- cell death
- germ cell
- metabolic syndrome
- risk assessment
- drug induced
- poor prognosis
- high resolution
- heavy metals
- cell cycle arrest
- heat shock
- drug delivery
- adipose tissue
- insulin resistance
- body mass index
- heat shock protein