Bułdak Rafał Jakub, Pilc-Gumuła Katarzyna, Bułdak Łukasz, Witkowska Daria, Kukla Michał, Polaniak Renata, Zwirska-Korczala Krystyna
Department of Physiology, School of Medicine with the Division of Dentistry, Medical University of Silesia, Zabrze 41‑808, Poland.
Department of Internal Medicine and Clinical Pharmacology, School of Medicine, Medical University of Silesia, Katowice 40‑752, Poland.
Mol Med Rep. 2015 Aug;12(2):2275-82. doi: 10.3892/mmr.2015.3599. Epub 2015 Apr 7.
Obesity is associated with an increased risk of certain types of cancer, including colon cancer. Adipose tissue is an endocrine organ that produces biologically active substances, such as leptin and ghrelin. Recent research has suggested that adipose-derived hormones may be associated with mechanisms linked to tumorigenesis and cancer progression. Furthermore, previous studies have demonstrated that pineal gland-derived melatonin possesses important oncostatic and antioxidant properties. The present study aimed to determine the effects of the adipokines ghrelin and leptin, and the melatonin on intracellular levels of reactive oxygen species (ROS) and the activity of selected antioxidant enzymes, such as superoxide dismutase, catalase (CAT) and glutathione peroxidase. The effects of these compounds were also determined on the viability of HCT 116 human colorectal carcinoma cells in vitro. The pro-oxidant and growth inhibitory effects of melatonin resulted in an accumulation of ROS and decreased antioxidant capacity in melatonin-treated cells. Ghrelin administration alone caused a significant decrease in the levels of ROS, due to an increased activity of CAT in the HCT 116 cells. In addition, the present study observed increased lipid peroxidation following melatonin treatment, and decreased levels of malondialdehyde following ghrelin or leptin treatment. In conclusion, ghrelin, leptin and melatonin have various influences on the antioxidant capacity of HCT 116 cells. Compared with the adipokines, treatment with melatonin increased ROS levels and decreased cellular viability.
肥胖与某些类型癌症(包括结肠癌)的风险增加有关。脂肪组织是一种能产生生物活性物质(如瘦素和胃饥饿素)的内分泌器官。最近的研究表明,脂肪衍生激素可能与肿瘤发生和癌症进展的相关机制有关。此外,先前的研究表明,松果体衍生的褪黑素具有重要的抑癌和抗氧化特性。本研究旨在确定脂肪因子胃饥饿素和瘦素以及褪黑素对细胞内活性氧(ROS)水平和所选抗氧化酶(如超氧化物歧化酶、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶)活性的影响。还测定了这些化合物对体外培养的HCT 116人结肠癌细胞活力的影响。褪黑素的促氧化和生长抑制作用导致褪黑素处理的细胞中ROS积累和抗氧化能力下降。单独给予胃饥饿素会导致ROS水平显著降低,这是由于HCT 116细胞中CAT活性增加所致。此外,本研究观察到褪黑素处理后脂质过氧化增加,而胃饥饿素或瘦素处理后丙二醛水平降低。总之,胃饥饿素、瘦素和褪黑素对HCT 116细胞的抗氧化能力有多种影响。与脂肪因子相比,褪黑素处理会增加ROS水平并降低细胞活力。