Nicotine is the more abundant and most significant components of cigarette smoke.
Epidemiological evidence strongly suggests an association between cigarette smoking
and pancreatic injury. Although effects of smoking on endocrine pancreas are still
controversial Here, we examined the impact and underlying mechanisms of action of
folic acid and vitamin B12 on nicotine induced damage in pancreatic islets of rats.
Male Wistar rats were treated with nicotine (3mg/kg body weight/day, intraperitonealy)
with or without folic acid (36μg/kg body weight/day, orally) and vitamin B12 (0.63μg/kg
body weight/day, orally) for 21days. Supplementation with folic acid and vitamin B12
suppressed the nicotine induced changes in HbA1c, insulin, TNF-α, IL-6, generation
of reactive oxygen species, and attenuated the changes in markers of oxidative stress.
Moreover, folic acid and vitamin B12 also counteracted the increased expression of
protein and mRNA contents of TNF-α and iNOS produced by nicotine. Further, folic acid
and vitamin B12 in combination limits the nicotine induced changes in cell cycle and
excessive apoptosis of the pancreatic β-cells and also successfully blunted the nicotine
induced alteration in loss of mitochondrial membrane potential. In conclusion, data
demonstrate that folic acid and vitamin B12 may be possible nutritional intervention
against cellular oxidative stress, which is a critical step in nicotine-mediated islet
injury, and improves islet cell functional status by scavenging free radicals and
by inhibiting the generation of pro-inflammatory mediators.