Laboratório de Biomedicina Translacional, Programa de Pós-Graduação em Ciências da Saúde, Universidade do Extremo Sul Catarinense - UNESC, Criciúma, Brazil.
Laboratório de Fisiopatologia Exprimental, Programa de Pós-Graduação em Ciências da Saúde, Universidade do Extremo Sul Catarinense - UNESC, Criciúma, Brazil.
Drug Chem Toxicol. 2022 Mar;45(2):515-522. doi: 10.1080/01480545.2020.1726380. Epub 2020 Feb 17.
Melanoma, an aggressive skin cancer originating from melanocytes, can metastasize to the lungs, liver, cortex, femur, and spinal cord, ultimately resulting in DNA mutagenic effects. Melatonin is an endogenous hormone and free radical scavenger that possesses the ability to protect the DNA and to exert anti-proliferative effects in melanoma cells. The aim of this study was to evaluate the effects of B16F10 melanoma cells and the effects of melatonin supplementation on genotoxic parameters in murine melanoma models. Thirty-two male C57Bl/6 mice were divided in the following four groups: PBS + vehicle ( = 6), melanoma + vehicle ( = 10), PBS + melatonin ( = 6), and melanoma + melatonin ( = 10). The melanoma groups received a B16F10 cell injection, and melatonin was administered during 60 days. After treatment, tumor sizes were evaluated. DNA damage within the peripheral blood, lungs, liver, cortex, and spinal cord was determined using comet assay, and the mutagenicity within the bone marrow was determined using the micronucleus test. B16F10 cells effectively induced DNA damage in all tissues, and melatonin supplementation decreased DNA damage in the blood, liver, cortex, and spinal cord. This hormone exerts anti-tumor activity via its anti-proliferative, antioxidative, and pro-apoptotic effects. As this result was not observed within the lungs, we hypothesized that melatonin can induce apoptosis in cancer cells, and this was not evaluated by comet assay. This study provides evidence that melatonin can reduce the genotoxicity and mutagenicity caused by B16F10 cells.
黑色素瘤是一种起源于黑素细胞的侵袭性皮肤癌，可转移到肺部、肝脏、大脑皮层、股骨和脊髓，最终导致 DNA 诱变效应。褪黑素是一种内源性激素和自由基清除剂，具有保护 DNA 和在黑色素瘤细胞中发挥抗增殖作用的能力。本研究旨在评估 B16F10 黑色素瘤细胞的作用以及褪黑素补充对小鼠黑色素瘤模型遗传毒性参数的影响。32 只雄性 C57Bl/6 小鼠分为以下四组：PBS+载体（ = 6）、黑色素瘤+载体（ = 10）、PBS+褪黑素（ = 6）和黑色素瘤+褪黑素（ = 10）。黑色素瘤组接受 B16F10 细胞注射，并在 60 天内给予褪黑素。治疗后，评估肿瘤大小。使用彗星试验测定外周血、肺、肝、大脑皮层和脊髓内的 DNA 损伤，并用微核试验测定骨髓内的诱变作用。B16F10 细胞有效地诱导了所有组织中的 DNA 损伤，褪黑素补充降低了血液、肝脏、大脑皮层和脊髓中的 DNA 损伤。这种激素通过其抗增殖、抗氧化和促凋亡作用发挥抗肿瘤活性。由于在肺部未观察到这种结果，我们假设褪黑素可以诱导癌细胞凋亡，而彗星试验未对此进行评估。本研究提供了证据表明，褪黑素可以降低 B16F10 细胞引起的遗传毒性和致突变性。
