ABSTRACT

Artificial Light at Night (ALAN) causes alteration in the redox status and membrane-bound transporters. Melatonin has pleiotropic effects on normal physiology and acts as a potential antioxidant. This study was undertaken to evaluate the effects of ALAN-induced alterations in the membrane transporters, oxidative stress biomarkers and to evaluate the protective effects of melatonin supplementation prior to exposure of light in a circadian-disrupted model of rat. Young male Wistar rats 250 ± 20 g were randomly segregated into following groups; Group (I) control, Group (II) melatonin-treated group (10 mg/kg, orally), Group (III) ALAN (500 lux), Group (IV) ALAN with melatonin, for 10 days. Results show that melatonin is an effective mediator of membrane-bound transporters revealed by activation of Na⁺/K⁺-ATPase (NKA), plasma membrane Ca²⁺-ATPase (PMCA) and suppression of Na⁺/H⁺ exchanger (NHE) activity. Oxidative stress biomarkers such as total thiol (T-SH), sialic acid (SA), lipid hydroperoxides (LHs) and protein carbonylation (PC) are also restored to the normal level after supplementation of melatonin. These findings demonstrate the protective effect of melatonin on membrane-bound enzymes along with other oxidative stress biomarkers against light-mediated oxidative damage in erythrocyte membrane.

摘要

夜间人工光 (ALAN) 会导致氧化还原状态和膜结合转运蛋白的改变。褪黑激素对正常生理具有多效作用，并作为一种潜在的抗氧化剂。本研究旨在评估 ALAN 诱导的膜转运蛋白、氧化应激生物标志物改变的影响，并在昼夜节律紊乱的大鼠模型中评估在光照前补充褪黑激素的保护作用。将250±20g的年轻雄性Wistar大鼠随机分成以下组；(I) 组对照、(II) 组褪黑激素治疗组 (10 mg/kg, 口服)、(III) 组 ALAN (500 勒克斯)、(IV) 组 ALAN 与褪黑激素, 10 天。结果表明，褪黑激素是通过激活 Na ⁺ /K揭示的膜结合转运蛋白的有效介质⁺ -ATPase (NKA)、质膜 Ca ²⁺ -ATPase (PMCA) 和抑制 Na ⁺ /H ⁺交换器 (NHE) 活性。补充褪黑激素后，总硫醇 (T-SH)、唾液酸 (SA)、脂质氢过氧化物 (LHs) 和蛋白质羰基化 (PC) 等氧化应激生物标志物也恢复到正常水平。这些发现证明了褪黑激素对膜结合酶以及其他氧化应激生物标志物对红细胞膜中光介导的氧化损伤的保护作用。