Ascorbic acid improves mitochondrial function in liver of arsenic-treated rat.

Area of Science:

• Biochemistry
• Toxicology
• Cell Biology

Background:

• Arsenic is a carcinogenic metalloid, primarily encountered through contaminated drinking water.
• Arsenic toxicity mechanisms involve inhibiting cellular respiration and causing mitochondrial damage.
• Ascorbic acid (vitamin C) is a water-soluble antioxidant that protects cells from oxidative stress.

Purpose of the Study:

• To investigate the protective effects of ascorbic acid against arsenic trioxide (As(III))-induced liver injury in rats.
• To evaluate the impact of ascorbic acid on mitochondrial function, oxidative stress markers, and apoptosis in arsenic-exposed livers.

Main Methods:

• Rats were treated with arsenic trioxide (As(III)) and co-treated with ascorbic acid.
• Assessed mitochondrial structure and function, including oxidative phosphorylation, adenosine triphosphatase (ATPase) activity, and succinic dehydrogenase activity.
• Measured caspase-3 activity and evaluated apoptosis and DNA damage.

Main Results:

• Co-treatment with ascorbic acid improved mitochondrial structure and function in As(III)-exposed livers.
• Ascorbic acid normalized ATPase activity, improved the ADP:O ratio, and restored succinic dehydrogenase activity.
• Ascorbic acid inhibited caspase-3, restricted apoptosis, and protected DNA from reactive oxygen species damage.

Conclusions:

• Ascorbic acid demonstrates a significant protective role against As(III)-induced liver injury.
• The antioxidative properties of ascorbic acid are key to mitigating arsenic toxicity.
• Ascorbic acid supports mitochondrial health and prevents arsenic-mediated cellular damage.