Acute or long-term exposure to N,N-dimethylformamide (DMF) can induce abnormal liver function. It is well known that DMF is mainly metabolized in the liver and thereby produces reactive oxygen species (ROS). The base excision repair (BER) pathway is regarded as a very important pathway involved in repairing ROS-induced DNA damage. Several studies have explored the associations between GSTM1, GSTT1, CYP2E1 polymorphisms and DMF-induced abnormal liver function; however, little is known about how common hOGG1, XRCC1 and APE1 polymorphisms and DMF induce abnormal liver function. The purpose of this study was to investigate whether the polymorphisms in the hOGG1 (rs159153 and rs2072668), XRCC1 (rs25487, rs25489, and rs1799782), APE1 (rs1130409 and 1760944) genes in the human BER pathway were associated with the susceptibility to DMF-induced abnormal liver function in a Chinese population. These polymorphisms were genotyped in 123 workers with DMF-induced abnormal liver function and 123 workers with normal liver function. We found that workers with the APE1 rs1760944 TG/GG genotypes had a reduced risk of abnormal liver function, which was more pronounced in the subgroups that were exposed to DMF for G polymorphism may be associated with DMF-induced abnormal liver function in the Chinese Han population.

Male reproductive disorders and declining fertility rates play an important role in birth rates, and their impact on future populations makes them one of the most serious public health issues of this century. Defects in spermatogenesis are the most common manifestation of male infertility, and exposure to environmental pollutants has been suggested as a potential cause. Nanomaterials, due to their unique physicochemical properties and widespread application, have raised growing concerns about their potential reproductive toxicity. Studies have shown that nickel nanoparticles (Ni NPs) have reproductive toxicity in male rats and mice, especially sperm damage. This study aimed to explore the male reproductive toxicity of Ni NPs and the role of mitochondrial fission in mouse spermatocytes (GC-2). Our results showed that Ni NPs induced the damage of mitochondrial structure and function in GC-2 cells and disrupted intramitochondrial homeostasis, thereby resulting in enhanced Dynamin-related protein 1(Drp1)-mediated mitochondrial fission and cell apoptosis, along with aggravated cytotoxicity and obvious reproductive toxicity. The mitochondrial division inhibitor 1(Mdivi-1) and lentiviral-transfected low expression of Dnm1l can significantly alleviate the germ cell toxicity caused by Ni NPs, suggesting a certain therapeutic effect. The novelty of this study lies in its systematic demonstration that Drp1-mediated mitochondrial division is a core pathogenic mechanism of Ni NP-induced male reproductive toxicity, and the validation of both pharmacological inhibition and genetic silencing as effective intervention strategies. Therefore, this study offers a reference for expanding the reproductive toxicity effect of Ni NPs and potential molecular mechanisms and provides an important basis for finding potential targets and treatment of Ni NPs.