Cadmium Induced Oxidative Damage Of Goattrophoblast Cells And The Protective Effects Of Nano Selenium

Cadmium?Cd?is a bio-accumulative toxic heavy metal pollutant that pollutes the environment mainly through the discharge of industrial wastewater,waste gas and waste residue.Previous studies showed that Cd is mainly enriched through the food chain,and threats multiple organs such as kidneys,livers and bones.Cd is more likely to accumulate in pregnant females and causes placental damage,which ultimately lead to fetal growth retardation,or even abortion.In the process of animal husbandry,Cd is mainly enrichedthrough ingesting Cd-contaminated grass,water and feed additives,and then causes dysfunction of some organs,and ultimately affects animal productivity and reproductive capacity.Goats are important economic animals in China,and reduced reproductive capacity caused by Cd seriously affects the development of goat husbandry and must be paid great attention.In this study,goat trophoblast cells?GTCs?were used to explore the molecular mechanisms of Cd-induced GTCs oxidative damage and the protective effects of nano-selenium?Se NPs?.These findings provide some ideas for the treatment of Cd-induced degradation of animal reproductive capacity,and have certain practical significance in guiding animal husbandry.Theexperimentalresultsareas follows:1.MTT results showed that CdCl₂ suppressed GTCs cell viability and inhibited cell growth in a time-and dose-dependent manner.Results showed that the cell became shrink,and exfoliated from dishes after CdCl₂ treatment.Both DCFH-DA fluorescence staining and flow cytometry showed that the intracellular reactive oxygen species?ROS?levels increased significantly after CdCl₂ treatment.Meanwhile,CdCl₂ treatment inhibited the activity of superoxide dismutase?SOD?,catalase?CAT?and glutathione peroxidase?GSH-Px?in GTCs.In addition,the intracellularmalonaldehyde?MDA? content increased significantly,indicating that CdCl₂ causes lipid peroxidation in GTCs.2.JC-1 fluorescence staining and flow cytometry showed that mitochondrial membrane potential was decreased significantly in GTCs after CdCl₂ treatment.Comet assay showed that CdCl₂ induced DNA damage in GTCs.Afterwards,results fromflow cytometry showed that CdCl₂ treatment caused cycle arrest in G0/G1 phase.DAPI staining and Annexin V-FITC/PIstaining showed that chromatin condensation,DNA fragmentation and apoptosis occurred in GTCs after CdCl₂ treatment.3.Compared with the CdCl₂ treatment group,Se NPs rescued the viability of CdCl₂-treated GTCs,and the morphology of GTCs resembled the typical epithelial-like cells.Furthermore,it was observed that Se NPs significantly inhibited the production of ROS and the decrease of mitochondrial membrane potential in GTCsafter CdCl₂ treatment.In addition,results from comet assay and flow cytometry showed that Se NPs significantly alleviated CdCl₂ induced DNA damage and apoptosis in GTCs.The results show that Se NPs significantly inhibit the oxidative damage in GTCs induced by CdCl₂.Inconclusion:CdCl₂ triggers oxidative stress mediated mitochondrial injury and apoptosis in goat trophoblast cells.These findingsin our study provided a theoretical basis for elucidating the pathogenic mechanism of Cd-induced abortion in mammals.Meanwhile,these findings may provide some ideas for the treatment of Cd-induced degradation of animal reproductive capacity,and have certain practical significance in guiding animal husbandry.