Sodium arsenite-induced cardiovascular and renal dysfunction in rat via oxidative stress and protein kinase B (Akt/PKB) signaling pathway.
Ademola Adetokunbo OyagbemiTemidayo Olutayo OmobowaleEbunoluwa Racheal AsenugaGrace Onyeche OchigboAbiola Olumuyiwa AdejumobiAdeolu Alex AdedapoMomoh Audu YakubuPublished in: Redox report : communications in free radical research (2017)
Exposure to arsenic caused a significant increase in malondialdehyde, H2O2 generation but decrease total thiol and reduced glutathione levels in both cardiac and renal tissues. Furthermore, increases in superoxide dismutase, glutathione-S-transferase and catalase with significant increases in glutathione peroxidase activities were observed in the cardiac tissues. On the contrary, a significant reduction in the renal antioxidant enzyme activity was recorded following exposure. Also, antioxidant defense system did not return to apparent values after arsenic withdrawal. Immunohistochemistry revealed a reduction in the expression of the pro-survival protein-protein kinase B (Akt/PKB) following exposure to arsenic and this was not reversed by withdrawal Discussion: Exposure to arsenic caused cardio-renal toxicity via induction of oxidative stress and down-regulation of Akt/PKB expressions.
Keyphrases
- oxidative stress
- signaling pathway
- diabetic rats
- drinking water
- protein kinase
- induced apoptosis
- heavy metals
- cell proliferation
- dna damage
- ischemia reperfusion injury
- pi k akt
- left ventricular
- hydrogen peroxide
- gene expression
- anti inflammatory
- poor prognosis
- epithelial mesenchymal transition
- heart failure
- high glucose
- binding protein
- risk assessment
- small molecule
- endoplasmic reticulum stress
- stress induced
- protein protein