Zongping Liu

Emerging as pervasive pollutants, microplastics (MPs) and cadmium (Cd) endanger animals’ health and safety. Currently, there is a lack of evidence about the harm mechanism of coexposure to polyvinyl chloride microplastics (PVC-MPs) and Cd in the avian female reproductive system. In the current study, female Mallard ducks were used to investigate a novel developmental reproductive toxicity strategy related to glycolipid metabolism disorder in duck follicles induced by coexposure to PVC-MPs with Cd, which leads to developmental reproductive toxicity. The findings demonstrated that coexposure to PVC-MPs and Cd enhanced PVC-MP accumulation in ovarian tissue, which impacted granulosa cell (GC) shape and functional activity and hindered folliculogenesis. Coexposure to PVC-MPs with Cd decreased the secretion of glycoprotein of zona pellucida (ZP) secreted by oocytes. Furthermore, coexposure to PVC-MPs with Cd increased oxidative stress (protein carbonyl content (PCC), H2O2) and decreased antioxidative stress (malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT)) enzyme activity in the ovary. Moreover, coexposure to PVC-MPs and Cd markedly enhanced the production of collagen fibers and stimulated the immunosignaling of transforming growth factors-β (TGF-β) and α-smooth muscle actin (α-SMA). Moreover, coexposure to PVC-MPs with Cd induced metabolic disorder of glycolipid proteins glucose transporter 8 (GLUT8), phosphoenolpyruvate carboxykinase (PCK2), triglyceride lipase (ATGL), carnitine palmitoyltransferase 2 (CPT2), and iron overload in the ovary. This work demonstrated that coexposure to PVC-MPs and Cd caused developmental reproductive toxicity in female ducks by triggering oxidative stress and altering glycolipid metabolic proteins. These results provide a novel study avenue for investigating the reproductive harmful mechanisms of PVC-MPs and Cd in bird species.

Cadmium (Cd) is a widespread environmental contaminant related to renal immunosuppression and metabolic dysfunction. Lycium barbarum polysaccharides (LBPs) are active extracts of wolfberry and possess a variety of excellent properties. However, the specific mechanism of action for Cd and LBP remain unclear. In the present study, Shaoxing ducks were used to establish an in vivo model to elucidate the effects of combined Cd and LBP exposure on the kidneys and the underlying mechanisms. The ducks were exposed to CdCl ₂ (50 mg/kg) and/or LBP (50 mg/kg) for 30 days. We observed that Cd exposure increased the kidney index and the levels of the renal function indicators CREA and UA. Further research revealed that Cd exposure caused histopathological damage and ultrastructural alterations. In addition, Cd accumulation induced oxidative stress by disrupting ionic homeostasis and inhibiting the Nrf2-mediated antioxidant defense pathway. Finally, we found that Cd promoted lipid accumulation, disrupted lipid metabolism, and thereby induced renal immunosuppression. Notably, LBP effectively alleviated Cd-induced renal injury, suggesting beneficial effects against Cd-triggered nephrotoxicity.

Introduction: Nanoplastics (NPs) can act as carriers for heavy metals, and co-exposure to NPs and co-pollutants may produce greater toxicity than single exposure. However, the combined toxicity of nanoplastics and heavy metals in poultry liver cells remains poorly understood. Methods: Primary duck embryonic hepatocytes (PDEH) were used as an in vitro model. Cells were exposed to polystyrene nanoplastics (PS-NPs, 80 nm, 10 μg/mL) and/or cadmium chloride (CdCl2, 4 μg/mL) for 12 h. Pyroptosis- and apoptosis-associated endpoints were assessed by brightfield microscopy, PI staining, SEM, flow cytometry, qRT-PCR, and Western blotting. The antioxidant N-acetylcysteine (NAC, 5 μg/mL) was used to evaluate the responses of these pathways. Results: Co-exposure to PS-NPs and Cd potentiated cadmium-induced pyroptosis-associated morphological changes, including cell swelling, rounding, membrane blebbing, and surface pore formation. Mechanistically, co-exposure activated the NLRP3/Caspase-1/GSDMD signaling axis, as indicated by increased NLRP3, cleaved Caspase-1 (P20/P10), GSDMD-NT, and intracellular IL-1β maturation. Co-exposure also exacerbated apoptosis-associated changes, including an increased Bax/Bcl-2 ratio and a higher Annexin V-positive cell population. NAC effectively reversed the apoptosis-associated endpoints but did not significantly alter the selected pyroptosis-associated markers under the present in vitro exposure conditions. Discussion: These findings suggest that PS-NPs potentiate Cd-induced hepatotoxicity in primary duck hepatocytes, with concurrent activation of pyroptosis- and apoptosis-associated signaling. The differential responses to NAC indicate that antioxidant intervention may preferentially attenuate apoptosis-associated injury under the present in vitro exposure conditions, while pyroptosis-associated signaling may require alternative targeted interventions. These results provide new insights into the combined toxicity of nanoplastics and heavy metals in avian hepatocytes.

Cadmium (Cd) is a neurotoxic heavy metal, and mitochondrial homeostasis disruption is a key mechanism underlying its neurotoxicity. SLC25A39, a mitochondrial transporter, maintains the mitochondrial homeostasis. This study investigated the role of SLC25A39 in the Cd-induced disruption of mitochondrial homeostasis in rat neuronal cells. The results revealed that Cd exposure markedly upregulated the SLC25A39 protein levels in neuronal cells. SLC25A39 deficiency further aggravated Cd-induced mitochondrial oxidative-stress-related abnormalities, including mitochondrial glutathione (mtGSH) depletion, elevated lipid peroxidation, mitochondrial reactive oxygen species (mtROS) accumulation, and reduced mitochondrial SOD2 protein levels. Moreover, SLC25A39 deficiency aggravated Cd-induced mitochondrial dysfunction, suppressed biogenesis, disrupted the dynamic balance, and hyperactivated mitophagy. Notably, DRP1 inhibition suppressed the Cd-induced upregulation of Pink1 and Parkin in SLC25A39-deficient PC12 cells. Collectively, SLC25A39 confers resistance to Cd-induced pleiotropic mitochondrial injuries, including oxidative stress, dysfunction, impaired biogenesis, dynamic imbalance, and excessive mitophagy. In PC12 cells, SLC25A39 may limit excessive mitophagy by negatively regulating the DRP1 activity.

Hydrogen sulfide (H ₂ S) is a pervasive environmental toxicant with well-established immunotoxic effects. However, its action on lymphoid organs—particularly whether it triggers splenic pyroptosis—remains elusive. This study explored the effect of acute H ₂ S exposure on rat spleen and the therapeutic potential of Xuebijing (XBJ), a traditional Chinese medicine for sepsis. Rats were exposed to 300 ppm H ₂ S for 3 h, with or without 7-day XBJ pretreatment (4 mg/kg, i.p.). Splenic injury was evaluated by histopathology, ultrastructure, oxidative stress parameters, immunofluorescence, and immunoblotting. H ₂ S exposure alone caused marked splenic damage, evidenced by increased organ coefficient, disrupted tissue architecture, mitochondrial swelling, and redox imbalance [depleted glutathione (GSH), superoxide dismutase (SOD), catalase (CAT); elevated malondialdehyde (MDA)]. Mechanistically, H ₂ S activated the NF-κB/NLRP3/caspase-1 axis, upregulating NLRP3, ASC, cleaved caspase-1, and GSDMD-N, along with elevated interleukin-1β (IL-1β) and interleukin-18 (IL-18). XBJ pretreatment reversed these alterations, suppressing NF-κB phosphorylation, inflammasome assembly, and pyroptotic cell death. These findings demonstrate that H ₂ S induces splenic pyroptosis via the NF-κB/NLRP3/caspase-1 pathway, and that XBJ confers protection by interrupting this cascade, offering a mechanism-based candidate for the treatment of acute H ₂ S poisoning.

Layer chickens have dual physiological demands for rapid growth and continuous egg production. The maintenance of skeletal homeostasis in layer chickens relies on the precise coordination among OCs, osteoblasts (OBs), and osteocytes. The imbalances in the supply of nutrients such as calcium (Ca) and phosphorus (P), as well as dysfunction of the “gut–bone” axis, can disrupt normal bone development in layer chickens, leading to bone diseases such as tibial dyschondroplasia (TD) and osteoporosis (OP), seriously damaging the production performance of layer chickens. This review systematically summarizes the knowledge background of the metabolic reprogramming of OCs in layer chickens, especially mitochondria-mediated biological processes, including oxidative phosphorylation (OXPHOS), glycolysis, reactive oxygen species (ROS) signaling, mitophagy, etc. Notably, the co-culture system of OCs derived from the bone marrow cavity of embryos in vitro has been established in laying chickens. However, there are few reports on the study of mitochondrial metabolism of OCs using this model. Therefore, this review particular focuses on the bone metabolism mediated by OCs in layer chickens and proposes future research priorities, including the application of gene editing and multi-omics methods to ultimately achieve targeted nutritional or pharmacological interventions for optimizing mitochondrial function and promoting bone health.