Effects of Environmental Arsenic Exposure on the Morphology of Multiple Organs in Female Mice During Pre‐Pregnancy, Gestation, and Lactation
Ying Xing, Shu Liu, Wenchao Liu, Chen Liang, Lijuan Zhang, Jianhai ZhangABSTRACT
To investigate the effects of environmentally relevant arsenic (As) exposure on multiple organs (liver, kidney, spleen, ovary, and uterus) in female mice during pre‐pregnancy, gestation, and lactation, and to clarify the critical time window associated with As‐induced organ toxicity. As exposure models (0.02, 0.1, or 0.5 mg/L As 2 O 3 ) were established for mice during pre‐pregnancy, gestation, and lactation. Meanwhile, the effects on the fertility of female mice, blood parameters, and pathological changes of the liver, kidneys, spleen, ovaries and uterus of the exposed mice were evaluated. Additionally, a marker of DNA‐strand break (γH2AX) and apoptosis (TUNEL) was assessed in the liver and kidney during gestation and lactation. The findings indicated that As exposure during these stages did not impair fertility in female mice. However, exposure to 0.5 mg/L As 2 O 3 during gestation caused reductions in red blood cells (RBC), hemoglobins (HGB), and platelets (PLT). Meanwhile, hepatic lipid levels was increased in mice exposure to 0.1 mg/L As 2 O 3 during gestation, and mice exposed to 0.1 mg/L As 2 O 3 during lactation exhibited glomerular atrophy and hepatocyte vacuolization. In addition, mice exposed to 0.5 mg/L As 2 O 3 during both gestation and lactation exhibited varying degrees of inflammatory cell infiltration in both the liver and kidney. Notably, γH2AX was elevated in the kidneys at 0.1 and 0.5 mg/L As 2 O 3 during gestation and lactation, whereas no change was observed in the liver. TUNEL staining revealed no obvious alterations in either organ throughout this period. These observations suggest that females may be more vulnerable to As during gestation and lactation, with the liver and kidney serving as primary sites of toxicity accumulation.