Cadmium induced cardiac toxicology in developing Japanese quail (Coturnix japonica): Histopathological damages, oxidative stress and myocardial muscle fiber formation disorder

ABSTR A C T The anthropogenic-induced cadmium (Cd) pollution poses great threats to human health and wildlife survival. Birds also suffer from Cd contamination and Cd exerts negative impacts on multiple organs in birds. However, its toxic effects on cardiac organ of birds are still unclear. In this study, one-week old male Japanese quails were exposed to 15, 30, 60 and 75 mg/kg Cd for 5 weeks when birds in control group reached sex maturity. The results showed that Cd could cause microstructural damages including congestion and myocardial fiberolysis. Ultra-structural analysis also showed myocardial muscle fiber disarrangement and rupture as well as mitochondrial swelling, vacuolation and membrane lysis in Cd concentration groups. Moreover, Cd induced oxidative stress in the heart by decreasing antioxidant enzyme activities of catalase (CAT), glutathione peroxidase (GPX), total antioxidant capacity (T-AOC), superoxide dismutase (SOD) while increasing oxidative biomarkers such as malondialdehyde (MDA), inducible nitric oxide synthase (iNOS), and content of nitric oxide (NO). In addition, mRNA expression levels of genes involved in muscle fiber formation signaling pathway such as Follistatin (FST), paired box 3 (PAX3), myogenic differentiation 1 (MYoD1) and SRY-box transcription factor 6 (SOX6), were down-regulated by Cd exposure. Furthermore, PI3K/Akt/mTOR signaling pathway were disrupted by Cd exposure implying energy supply deficiency in the heart. We concluded that Cd caused cardiac dysfunction by inducing heart underdevelopment, histopathological injury, oxidative stress and myocardial muscle fiber for-mation disruption.

Automated summary

This study revealed that Cd pollution could result in microstructural damages and oxidative stress in the hearts of birds, affecting gene expression levels related to muscle fiber formation signaling pathway, leading to cardiac dysfunction.