Impact of HIF1-α/TGF-β/Smad-2/Bax/Bcl2 pathways on cobalt chloride-induced cardiac and hepatorenal dysfunction.

Background: Cobalt chloride (CoCl) is a ferromagnetic ubiquitous trace element extensively dispersed in the environment. Nevertheless, it may merit human hazard.

Aim: Excess cobalt can harm vital organs this paves the way to elucidate the toxic impact of CoCl on the liver, kidney and heart.

Method: CoCl was injected in a dose of (60 mg/kg, S.C.) proceeded via Carnosine (200 mg/kg) and/or Arginine (200 mg/kg) treatment 1 month, 24 and 1 h, prior to CoCl-intoxication.

Results: CoCl significantly alleviated hemoglobin concentration and BCl2; meanwhile, protein expression of transforming growth factor (TGF-β), hypoxia-inducible factor (HIF-1α), Mothers against decapentaplegic (Smad-2), AKT protein expression and Bax/Bcl2 ratio was noticeably elevated.

Conclusion: The combination of the aforementioned antioxidants exerted a synergistic anti-apoptotic impact in all target tissues.