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首页> 外文期刊>Photodermatology, photoimmunology and photomedicine >Phototoxicity to diuretics and antidiabetics in the cultured keratinocyte cell line HaCaT: evaluation by clonogenic assay and single cell gel electrophoresis Comet assay).
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Phototoxicity to diuretics and antidiabetics in the cultured keratinocyte cell line HaCaT: evaluation by clonogenic assay and single cell gel electrophoresis Comet assay).

机译：在培养的角质形成细胞系HaCaT中对利尿剂和抗糖尿病药的光毒性：通过克隆形成测定和单细胞凝胶电泳彗星测定进行评估）。

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BACKGROUND: Potential phototoxicity has been described for a number of drugs and chemical substances. Psoralens, chlorpromazines and fluoroquinolones have been described as inducing photomutagenicity and photocarcinogenicity in vitro and in vivo. We wanted to investigate oral antidiabetics and diuretics for potential phototoxicity and possible DNA damage in the HaCaT cell line. METHODS: : The oral antidiabetics tolbutamide, glibenclamide and glipizide, and the diuretics bendroflumethiazide, butizide, furosemide, hydrochlorothiazide and trichlormethiazide were dissolved in DMSO to final concentrations of 1 mM, 0.1 mM, and 0.01 mM, incubated together with the cells, and exposed to UVA1 (23 or 48 J/cm2). Cell survival was evaluated in a clonogenic assay and phototoxic DNA damage was investigated by single cell gel electrophoresis (comet assay). To investigate possible inhibiting effects of antioxidants, L-ascorbic acid and alpha-tocopherol were added at a final concentration of 1 mM 24 h before treatment with the drugs. RESULTS: Bendroflumethiazide, furosemide, hydrochlorothiazide, trichlormethiazide and tolbutamide induced dose-dependent phototoxicity in the clonogenic assay. Cells incubated with bendroflumethiazide, tolbutamide and glibenclamide and irradiated with UVA1 demonstrated increased oxidative DNA damage, revealed as alkali-labile sites in the comet assay. Pretreatment with L-ascorbic acid or alpha-tocopherol suppressed the UVA-induced DNA damage in cells incubated with 1 mM bendroflumethiazide, furosemide, glibenclamide, glipizide, tolbutamide or trichloromethiazide. CONCLUSION: Several oral antidiabetics and diuretics show phototoxic effects in the HaCaT cell line. Inhibiting effects of antioxidants point towards involvement of reactive oxygen species in phototoxic DNA damage, suggesting a link between the phototoxic and photocancerogenic potential of the sulfonamide-derived oral antidiabetic and diuretic drugs. Excessive exposure to UV light may be deleterious for patients treated with oral antidiabetic and diuretic drugs.
机译：背景：已经描述了许多药物和化学物质的潜在光毒性。补骨脂素，氯丙嗪和氟喹诺酮类药物已被描述为在体外和体内诱导光致突变性和光致癌性。我们想研究HaCaT细胞系中潜在的光毒性和可能的​​DNA损伤的口服降糖药和利尿剂。方法：将口服降糖药甲苯磺丁胺，格列本脲和格列吡嗪，以及利尿剂苯溴氟甲肼，丁嗪，呋塞米，氢氯噻嗪和三氯甲嗪溶解在DMSO中，使其最终浓度分别为1 mM，0.1 mM和0.01 mM，与细胞一起孵育并暴露达到UVA1（23或48 J / cm2）。通过克隆形成测定评估细胞存活，并通过单细胞凝胶电泳（彗星测定）研究光毒性DNA损伤。为了研究抗氧化剂的可能抑制作用，在用药物治疗前24小时以1 mM的最终浓度添加了L-抗坏血酸和α-生育酚。结果：在成克隆试验中，苯氟甲酰肼，呋塞米，氢氯噻嗪，三氯甲酰肼和甲苯磺丁酰胺引起剂量依赖性光毒性。用苯达氟甲酰肼，甲苯磺丁酰胺和格列本脲孵育并用UVA1照射的细胞显示出增加的氧化DNA损伤，在彗星测定中显示为碱不稳定位点。用L-抗坏血酸或α-生育酚预处理可抑制UVA诱导的DNA损伤，该细胞与1 mM苯达氟甲酰肼，速尿，格列苯脲，格列吡嗪，甲苯磺丁酰胺或三氯甲酰肼孵育。结论：几种口服降糖药和利尿剂对HaCaT细胞系具有光毒性作用。抗氧化剂的抑制作用表明活性氧参与了光毒性DNA损伤，这表明磺酰胺类口服降糖药和利尿药的光毒性和光致癌性之间存在联系。对于口服抗糖尿病药和利尿药治疗的患者，过度暴露于紫外线可能有害。

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