Abstract
Purpose: :
To study the effects of hydroquinone (HQ), one of the toxic components of cigarette smoke, on human retinal Müller cells (MIO-M1).
Methods: :
MIO-M1 cells were treated for 24 hours with 200 µM, 100 µM, 50 µM, and 25 µM of HQ. Cell viability was measured by a trypan blue dye exclusion assay. Mitochondrial dehydrogenase activity was evaluated by WST- 1 assay.
Results: :
Mean cell viabilities of MIO-M1 cells after exposure to 200 µM, 100 µM, 50 µM, and 25 µM of HQ were 41.8% ± 0.31 (P<0.001), 49.96% ± 1.72 (P<0.001), 65.07% ± 0,45 (P<0.001) and 71.13% ± 0.27 (P 0.001) respectively. Mean cell viability of DMSO equivalents and untreated MIO-M1 cells were 73.2% ± 0.44, 74.7% ± 0.08, 79.89% ±1.06, 76.18%± 0.45 and 93.53 %± 0.27 respectively. A decrease in mitochondrial dehydrogenase activity compared to DMSO equivalents and untreated cells as measured by decrease in absorbence values at OD 450 nm was found in MIO-M1 cells at all HQ concentrations tested .The mean absorbance values of Müller cells after 24 hours of exposure to 200 µM, 100 µM, 50 µM, and 25 µM HQ were 0.14 ± 0.0078 (P<0.05), 0.12 ± 0.047 (P<0.001), 0.29 ± 0.030 (P>0.05) and 0.28 ± 0.015 (P>0.05) respectively. Mitochondrial dehydrogenase activity at comparable DMSO concentrations were 0.20 ± 0.031, 0.25 ±0.012, 0.28±0.023, 0.25±0.012 respectively.In the untreated cells were 0.36± 0.31.
Conclusions: :
Cigarette smoking is a signifficant risk factor in AMD. Hydroquinone, a toxic component of cigarette smoke, was shown here to reduce cell viability and mitochondrial dehydrogenase activity on retinal Müller cells in vitro.
Keywords: drug toxicity/drug effects • retinal culture • age-related macular degeneration