Microcystins (MCs) and nitrites are coexisted in the environment and have reproductive toxicity. The combined toxic effect and mechanism of MCs and nitrite on spermatogenesis remain largely unclear. In the present study, co-exposure to microcystin-leucine arginine (MC-LR) and sodium nitrite (NaNO₂) aggravated testicular damage of Balb/c mice and mitochondrial impairment of spermatogonia, Sertoli cells, and sperm. Furthermore, MC-LR and NaNO₂ reduced sperm density with a synergistic effect. In addition, MC-LR and NaNO₂ synergistically induced oxidative stress in the reproductive system by decreasing superoxide dismutase (SOD) activity and glutathione (GSH) levels and increasing levels of mitochondrial reactive oxygen species (mtROS) and reactive oxygen species (ROS). More importantly, mitoquidone mesylate (MitoQ), an inhibitor of mtROS, blocked MC-LR and NaNO₂-induced spermatogonia and Sertoli cell apoptosis by inhibiting high expression of Bax, Fadd, Caspase-8, and cleaved-Caspase-3. On the other hand, MitoQ suppressed pyroptosis of Sertoli cells by inhibiting the expression of NLRP3, N-GSDMD, and cleaved-Caspase-1. Additionally, MitoQ alleviated co-exposure-induced sperm density reduction and organ index disorders in F1 generation mice. Together, co-exposure of MC-LR and NaNO₂ can enhance spermatogenic disorders by mitochondrial oxidative impairment-mediated germ cell death. This study emphasizes the potential risks of MC-LR and NaNO₂ on reproduction in realistic environments and highlights new insights into the cause and treatment of spermatogenic disorders.

Microplastics (MPs) and nanoplastics (NPs) are pervasive and persistent environmental pollutants raising growing concerns regarding their potential hazards to human respiratory health. This review systematically summarizes current epidemiological evidence and experimental findings concerning the respiratory toxicity of MPs and NPs. Exposure to these particles is associated with various pulmonary disorders, including pneumonia, chronic obstructive pulmonary disease, asthma, and other pathological lung injury. At the molecular level, MP- and NP-induced toxicity primarily involves oxidative stress, leading to mitochondrial dysfunction and endoplasmic reticulum stress. This oxidative damage triggers diverse forms of cell death, such as apoptosis, pyroptosis, ferroptosis, and autophagy. Furthermore, MPs and NPs induce pulmonary inflammation, disrupt the integrity of the alveolar-capillary barrier, promote pulmonary fibrosis, and cause DNA damage, mainly via oxidative stress pathways. This review also identifies critical directions for future research on the respiratory toxicity of MPs and NPs. Overall, this review highlights the respiratory health risks associated with MPs and NPs, emphasizing mechanisms involving oxidative stress, inflammation, and fibrosis, and underscores the urgent need for further investigation. It provides essential toxicological evidence and insights that could inform the development of effective protective strategies.

Background: Ambient ozone (O ₃ ) may adversely affect the upper airway, but whether temperature modifies its short-term association with outpatient visits for allergic rhinitis remains unclear. Methods: We conducted a time-stratified case-crossover study of 43,418 outpatient visits for allergic rhinitis at a tertiary hospital in Henan, China, during April–October of 2013–2023. Daily O ₃ , PM _2.5 , temperature, and relative humidity (RH) were assigned by residential address using gridded datasets and averaged over lag 0–1 day. Conditional logistic regression estimated odds ratios (ORs) and 95% confidence intervals (CIs) per 10 μg/m ³ increase in O ₃ across the observed exposure distribution, adjusting for temperature, RH, and PM _2.5 . Temperature modification was assessed using an interaction term between O ₃ and a natural cubic spline function of temperature. Results: Each 10 μg/m ³ increase in O ₃ was associated with a 1.2% increase in the odds of an outpatient visit for allergic rhinitis (OR = 1.012, 95% CI: 1.006–1.017). The largest age-specific estimate was observed among patients aged <18 years (OR = 1.030, 95% CI: 1.017–1.044). Temperature significantly modified the association (χ ² = 31.2, P < 0.001), the OR for O ₃ increased from 1.000 at the 25th percentile of temperature to 1.021 at the 75th percentile. Conclusion: Short-term O ₃ exposure was associated with higher odds of outpatient visits for allergic rhinitis, with larger estimates at higher temperatures and among patients aged <18 years.