Hexavalent chromium induced heart dysfunction via Sesn2-mediated impairment of mitochondrial function and energy...

Area of Science:

• Environmental toxicology
• Cardiovascular research
• Mitochondrial biology

Background:

• Hexavalent chromium (Cr(VI)) is a toxic industrial pollutant.
• Cr(VI) can damage heart cell membranes via lipid peroxidation.
• The precise mechanisms of Cr(VI)-induced heart dysfunction remain unclear.
• Sesn2 is an antioxidant molecule that protects against heart disease.

Purpose of the Study:

• To investigate the molecular mechanisms of heart dysfunction induced by chronic Cr(VI) exposure.
• To determine the role of Sesn2 in Cr(VI)-induced cardiotoxicity.

Main Methods:

• Wistar rats were exposed to potassium dichromate (K2Cr2O7) for 35 days.
• Evaluated hematological parameters, oxidative stress markers, cardiac structure, and function.
• Assessed cardiomyocyte apoptosis, ATP levels, mitochondrial integrity, and protein expression (Drp1, Bax, Mfn2, PGC-1α, Sesn2, Nrf2, HO-1, NQO1).

Main Results:

• Cr(VI) exposure led to dose-dependent hematological changes, oxidative stress, and cardiac dysfunction.
• Observed disorganized heart structure, cardiomyocyte apoptosis, ATP depletion, and mitochondrial impairment.
• Increased Drp1 and Bax expression, while Mfn2, PGC-1α, Sesn2, Nrf2, HO-1, and NQO1 protein levels were suppressed.

Conclusions:

• Chronic Cr(VI) exposure causes dose-dependent heart dysfunction in rats.
• The mechanism involves the loss of Sesn2, leading to impaired mitochondrial function and energy supply.
• Cr(VI) exposure disrupts mitochondrial dynamics and antioxidant defenses in the heart.