Cadmium exposure impairs porcine embryonic development by inducing oxidative stress and mitochondrial dysfunction

• Published in: Journal of animal reproduction & biotechnology (Online) Vol. 39; no. 1; pp. 48 - 57
• Main Authors: Kim, Min Ju, Jeon, Se‑Been, Kang, Hyo‑Gu, Song, Bong‑Seok, Sim, Bo‑Woong, Kim, Sun‑Uk, Jeong, Pil‑Soo, Cho, Seong‑Keun
• Format: Journal Article
• Language: English
• Published: 한국동물생명공학회(구 한국수정란이식학회) 31.03.2024; The Korean Society of Animal Reproduction and Biotechnology; 사단법인 한국동물생명공학회
• Subjects: cadmium; mitochondrial function; oxidative stress; porcine embryonic development; 축산학; cadmium; mitochondrial function; oxidative stress; porcine embryonic development
• ISSN: 2671-4639; 2671-4663
• DOI: 10.12750/JARB.39.1.48

Background: Cadmium (Cd) is toxic heavy metal that accumulates in organisms after passing through their respiratory and digestive tracts. Although several studies have reported the toxic effects of Cd exposure on human health, its role in embryonic development during preimplantation stage remains unclear. We investigated the effects of Cd on porcine embryonic development and elucidated the mechanism. Methods: We cultured parthenogenetic embryos in media treated with 0, 20, 40, or 60 μM Cd for 6 days and evaluated the rates of cleavage and blastocyst formation. To investigate the mechanism of Cd toxicity, we examined intracellular reactive oxygen species (ROS) and glutathione (GSH) levels. Moreover, we examined mitochondrial content, membrane potential, and ROS. Results: Cleavage and blastocyst formation rates began to decrease significantly in the 40 μM Cd group compared with the control. During post-blastulation, development was significantly delayed in the Cd group. Cd exposure significantly decreased cell number and increased apoptosis rate compared with the control. Embryos exposed to Cd had significantly higher ROS and lower GSH levels, as well as lower expression of antioxidant enzymes, compared with the control. Moreover, embryos exposed to Cd exhibited a significant decrease in mitochondrial content, mitochondrial membrane potential, and expression of mitochondrial genes and an increase in mitochondrial ROS compared to the control. Conclusions: We demonstrated that Cd exposure impairs porcine embryonic development by inducing oxidative stress and mitochondrial dysfunction. Our findings provide insights into the toxicity of Cd exposure on mammalian embryonic development and highlight the importance of preventing Cd pollution.