il\VOLVEMENT OF RETII\OIC ACID II{ - MSpace at the University of ...

(Kitamura et al. 2002). This inhibition of apoptosis was achieved by the retinoic acidinduced
suppression of c-fos/c-jun expression and the attenuation of JNK activation
(Kitamura et al. 2002). Another antioxidant protective mechanism of retinoic acid is the
activation of transcription of genes involved in the production of antioxidant enzymes'
Ahlemayer et al. (2001) has reported that the administration of all trans retinoic acid
(1nM-1pM) resulted in a complete prevention of staurosporine-induced oxidative stress
and apoptosis in cultured hippocampal neurons (Ahlemeyerp et al. 2001). This was
achieved by an increase in the Cu/Zn-SOD and Mn-SOD mRNA and protein expression
(Ahlemeyer et al. 2001).
Retinoic acid was also shown to protect against highly reactive NO radical. Alltrans
retinoic administration was able to decrease the NO production in bovine aortic
endothelial cells and this was achieved in a dose and time dependent manner (Cho et al'
2005). The data from this study did not show any alteration in the eNOS expression,
however it was reported that retinoic administration caused a reduction in eNOS-Serl179
phosphorylation which led to a decrease in the enzqe activation (Cho et al. 2005)' kt
this model, the administration of retinoic acid also resulted in a decrease in the expression
of vascular endothelial growth factor (VGF) and Akt phosphorylation (Cho et al. 2005).
The usage of RARcr antagonist did not block the inhibitory effects of all trans retinoic
acid, suggesting that these effects were not mediated by retinoic acid receptors (Cho et al.
2005). The antioxidant nature of retinoic acid is not only limited to its all-trans form, the
13-cis retinoic acid was also found to cause a protection against benzoyl peroxideinduced
oxidative stress on murine skin tissue. The administration of 13-cis retinoic acid
was found to recover depleted levels of glutathione and prevent an increase in the lipid
57