Purchase this article with an account.
Ben Davis, Kailin Tian, Lisa Turner, Shereen Nizari, Giulia Malaguarnera, M Francesca Cordeiro; CoQ10 reduces Vitamin E-TPGS toxicity effects in primary retinal cell culture. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):4958.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Recently, we reported that Vitamin E-TPGS could exacerbate the toxicity of dimethylsulfoxide (DMSO) in RGC-5 cells, through inhibition of the multidrug efflux channel P-glycoprotein (P-gp) (Butt et al, 2014. Invest Ophthalmol Vis Sci;55: E-Abstract 1709). The present study sought to determine whether a similar trend occurred in primary retinal cell cultures and whether CoQ10, which is a potential neuroprotective agent, could alter these changes.
Cell viability experiments were performed in the presence of DMSO and varying concentrations of vitamin E-TPGS and vitamin E-TPGS/CoQ10 in mixed retinal cultures and primary murine Retinal Ganglion Cells (RGCs). Cell survival was measured after 24h exposure to cytotoxic insults including DMSO and vitamin E-TPGS with or without CoQ10 using the AlamarBlue viability assay.
In agreement with previous results using immortalized cells, vitamin E-TPGS treatment of mixed retinal cultures was found to significantly exacerbate the toxicity of DMSO insult in a dose dependent manner (Pearson’s r=-0.9331, p=0.007). In contrast, CoQ10 treatment with Vitamin E-TPGS was found to abolish this effect (Pearson’s r=0.052, p=0.664). Similar results were obtained using primary RGC cultures.
Vitamin E-TPGS mediated P-gp inhibition was previously reported to increase immortalized retinal cell susceptibility to DMSO insult. The present study provides evidence to suggest a similar phenomenon occurs in primary retinal cultures. However, the presence of the antioxidant CoQ10 abolishes this effect, underlining its neuroprotective effects through different intracellular mechanisms.
This PDF is available to Subscribers Only