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• W2076154601 abstract "Smoking is a risk factor in the development of a variety of neuroretinal diseases. Therefore, we have investigated the effects of hydroquinone (HQ), a toxicant that is present in high concentrations in cigarette smoke, on a human retinal Müller cell line (MIO-M1). MIO-M1 cells were treated for 24 h with four different concentrations of HQ (200 μM, 100 μM, 50 μM, and 25 μM). Assays were used to measure cell viability, reactive oxygen/nitrogen species (ROS/RNS), mitochondrial dehydrogenase activity (WST assay), caspase-3/7 activity and lactate dehydrogenase (LDH) levels. Western blot analyses with anti-LC3 and anti-GAPDH antibodies were performed on HQ-treated samples. Some cultures were treated with 4 μM rapamycin, to induce autophagy, with and without the autophagy inhibitor 3-methyl-adenine (3MA), and levels of ROS/RNS and LDH were measured. Our findings show that HQ reduced cell viability at four different concentrations tested (200, 100, 50 and 25 μM); decreased mitochondrial function at concentrations of 200 and 100 μM; increased ROS/RNS activity at all the concentrations tested and increased LDH levels at concentrations of 200, 100 and 50 μM. Caspase-3/7 activities were not modified by HQ. However, treatment of these cells with this agent resulted in the appearance of the autophagy associated LC3-II band. Pre-treatment with 3MA reduced the ROS/RNS and LDH levels of the HQ-treated and rapamycin-treated cells. Our study suggests that HQ damages the MIO-M1 cells through oxidative, mitochondrial and autophagic pathways and not caspase-related apoptosis." @default.
• W2076154601 created "2016-06-24" @default.
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• W2076154601 date "2013-12-01" @default.
• W2076154601 modified "2023-10-01" @default.
• W2076154601 title "Hydroquinone induces oxidative and mitochondrial damage to human retinal Müller cells (MIO-M1)" @default.
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• W2076154601 doi "https://doi.org/10.1016/j.neuro.2013.08.004" @default.
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