This review summarizes the impact of tocotrienols (TCTs) as antioxidants in minimizing
oxidative stress (OS), particularly in embryos exposed to OS causing agents. OS level is
increased, for example, by nicotine, a major alkaloid content in cigarette, which is also a source
of exogenous reactive oxygen species (ROS). Increased nicotine-induced OS increases cell
stress response, which is a common trigger leading to embryonic cell death. Having more
profound anti-oxidative stress effects than its counterpart tocopherol, TCTs improve blastocyst
implantation, foetal growth, pregnancy outcome and survival of the neonates affected by
nicotine. In reversing cell developmental arrest caused by nicotine-induced OS, TCTs enhances
PDK-1 expression in the P13K/Akt pathway and permit embryonic development beyond the 4-
cell stage with the production of more morulae. At the cytoskeletal level, TCTs increase the
number of nicotine-induced apoptotic cells, through caspase 8 activation in the mitochondria.
TCTs facilitate rough endoplasmic reticulum (rER) stress-mediated apoptosis and autophagy,
resulting from nicotine-induced OS. Reduced vesicular population in TCT supplemented
oocytes on the other hand may suggest reduced secretion of apoptotic cell bodies thus probably
minimizing vesicular apoptosis during oocyte maturation. Further extensive research is
required to develop TCTs as a tool in specific therapeutic approaches to overcome the
detrimental effects of OS.
This review summarizes the impact of tocotrienols (TCTs) as antioxidants in minimizing oxidative stress (OS), particularly in embryos exposed to OS causing agents. OS level is increased, for example, by nicotine, a major alkaloid content in cigarette, which is also a source of exogenous reactive oxygen species (ROS). Increased nicotine-induced OS increases cell stress response, which is a common trigger leading to embryonic cell death. Having more profound anti-oxidative stress effects than its counterpart tocopherol, TCTs improve blastocyst implantation, foetal growth, pregnancy outcome and survival of the neonates affected by nicotine. In reversing cell developmental arrest caused by nicotine-induced OS, TCTs enhances PDK-1 expression in the P13K/Akt pathway and permit embryonic development beyond the 4-cell stage with the production of more morulae. At the cytoskeletal level, TCTs increase the number of nicotine-induced apoptotic cells, through caspase 8 activation in the mitochondria. TCTs facilitate rough endoplasmic reticulum (rER) stress-mediated apoptosis and autophagy, resulting from nicotine-induced OS. Reduced vesicular population in TCT supplemented oocytes on the other hand may suggest reduced secretion of apoptotic cell bodies thus probably minimizing vesicular apoptosis during oocyte maturation. Further extensive research is required to develop TCTs as a tool in specific therapeutic approaches to overcome the detrimental effects of OS.
Introduction: The present study aims to investigate the effects of nicotine on foetal loss,
postnatal growth and corresponding levels of oestrogen and progesterone in pregnant rats.
Methods: Subcutaneous injection of nicotine tartrate (7.5 mg/kg/day) was administered to
groups of pregnant rats; with treatment scheduled from day 1 through day 5, day 5 through
day 9 or day 1 through day 9 of pregnancy. On day 10 of pregnancy, laparotomy was
performed to count the number of blastocyst implantation sites. During parturition, the
number of viable pups was recounted and statistically compared with the controls. One
group of rats which received nicotine from day 1 through day 9 of pregnancy was sacrificed
on day 16 of pregnancy, and circulating levels of oestrogen and progesterone were
measured. Upon delivery, the birth weight of the pups was measured, and their weights were
recorded until weaning. Results: There was a significant increase in foetal loss particularly in
rats which received nicotine from day 5 through day 9 and from day 1 through day 9 of
pregnancy. There was also significantly lower birth weight of pups in all groups; however,
this pattern did not continue until weaning. Plasma oestrogen level was significantly elevated
with a significant decrease in the plasma progesterone level. Conclusions: Nicotine
administration during pregnancy showed an increase in foetal loss with a corresponding
increase in oestrogen and decrease in progesterone levels. Although the birth weight of the
pups was low, there was catch-up growth in the pups.