Targeting mitochondria with folic acid and vitamin B₁₂ ameliorates nicotine mediated islet cell dysfunction

Area of Science:

• Biochemistry
• Toxicology
• Cell Biology

Background:

• Nicotine, a toxic component of cigarette smoke, causes adverse health effects.
• Previous studies showed nicotine induces reactive oxygen species (ROS) and disrupts mitochondrial membrane potential (ΔΨm) in islet cells.
• Folic acid and vitamin B12 supplementation mitigated nicotine-induced pancreatic islet cell changes.

Purpose of the Study:

• To elucidate the toxicological effects and underlying mechanisms of nicotine-induced mitochondrial dysfunction in pancreatic islet cells.
• To investigate the protective role of folic acid and vitamin B12 against nicotine toxicity.

Main Methods:

• Assessed effects of nicotine on mitochondrial enzyme activities, cytosolic Ca2+ levels, ROS production, and oxidative stress markers (malondialdehyde, nitric oxide, glutathione).
• Evaluated changes in mitochondrial membrane potential (ΔΨm) and apoptosis-related proteins (Bcl-2, Bax, cytochrome c, caspase-9, PARP).
• Determined the protective effects of folic acid and vitamin B12 supplementation.

Main Results:

• Nicotine exposure decreased mitochondrial enzyme activities and antioxidant levels while increasing cytosolic Ca2+ and ROS production.
• Nicotine led to loss of ΔΨm, increased malondialdehyde and nitric oxide, and decreased glutathione.
• Nicotine induced islet cell apoptosis by modulating ΔΨm and altering apoptotic protein expressions, effects reversed by folic acid and vitamin B12.

Conclusions:

• Nicotine disrupts islet cell mitochondrial redox status and apoptotic machinery, leading to ΔΨm disruption.
• Folic acid and vitamin B12 supplementation effectively counteracted nicotine-induced mitochondrial alterations.
• This study provides insights into the pathophysiology of nicotine-mediated islet cell mitochondrial dysfunction.