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Volume 6, Issue 6(Suppl)
J Clin Toxicol 2016
ISSN: 2161-0495, JCT an open access journal
Page 56
Notes:
Euro Toxicology 2016
October 24-26, 2016
conferenceseries
.com
Toxicology & Applied Pharmacology
October 24-26, 2016 Rome, Italy
7
th
Euro-Global Summit on
Folic acid and vitamin B
12
as possible panacea against nicotine induced pancreatic β-cell
apoptosis and dysfunction
Sandip Mukherjee
and
Ankita Bhattacharjee
Serampore College, India
C
igarette smoking in regular habits affects our bodies in various ways and nicotine is the more abundant and most significant
components of cigarette smoke. Epidemiological evidence strongly suggests an association between cigarette smoking and
pancreatic injury. However, effects of cigarette smoking on pancreatic islets are still controversial. Impact and underlying
mechanism of actions of folic acid and vitamin B
12
on nicotine induced damage in pancreatic islets of rats are examined in the
present study. Male Wister rats were exposed to nicotine with or without supplementation of folic acid and vitamin B
12
. Folic
acid and vitamin B
12
,
in combination, blunted the nicotine induced impairment in glucose tolerance, and levels of HbA1c and
insulin in rats. Pro-inflammatory cytokines like TNF-α and IL-6, generation of reactive oxygen species, nitric oxide production
and other oxidative stress parameters were also attenuated by folic acid and vitamin B
12
in nicotine treated rats. Both, folic acid
and vitamin B
12
in combination also limits the nicotine induced changes in cell cycle and excessive apoptosis of the pancreatic
β-cell along with altered Bcl-2, Bax, caspase-3 and caspase-9 expression and up regulation of iNOS and TNF-α. Nicotine-
induced alteration in loss of mitochondrial membrane potential (Δψm) and release of cytochrome c also reversed by folic acid
and vitamin B
12
supplementation. In conclusion, folic acid and vitamin B
12
protects against islet cellular oxidative stress, which
is a critical step in nicotine-mediated islet injury, and improves islet cell functional status by scavenging free radicals, inhibiting
the generation of pro-inflammatory mediators and apoptosis.
Biography
Sandip Mukherjee received his PhD degree in the year 2007 from Jadavpur University, Kolkata, India and has published over 24 research articles and book
chapter. He is an Assistant Professor (Senior Grade) at Department of Physiology, Serampore College since 2008. He has been serving as Reviewer in different
international journals with repute.
sm_kdc@yahoo.co.inSandip Mukherjee et al., J Clin Toxicol 2016, 6:6(Suppl)
http://dx.doi.org/10.4172/2161-0495.C1.021