Damiani Adriani Paganini, Garcez Michelle Lima, Letieli de Abreu Larissa, Tavares Taís Helena, Rodrigues Boeck Carina, Moraes de Andrade Vanessa
a Laboratório de Biologia Celular e Molecular, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde , Universidade do Extremo Sul Catarinense - UNESC , Criciúma , SC , Brazil.
b Programa de Pós-graduação em Nanociências , Centro Universitário Franciscano - UNIFRA , Santa Maria , RS , Brazil.
J Toxicol Environ Health A. 2017;80(13-15):621-629. doi: 10.1080/15287394.2017.1286901. Epub 2017 May 19.
Studies on caffeine consumption have shown a negative correlation with development of some diseases with subsequent beneficial manifestations. Our aim was to assess the effects of caffeine on peripheral blood and neural tissue DNA in young adult and aged mice. Male Swiss mice (age 2-3 or 16-18 months, respectively) were treated with a caffeine solution (0.3 g/l) for 4 weeks, while controls received water. After the treatments, blood and hippocampal cells (for a comet assay) and femurs (for a micronucleus [MN] test) were collected. The comet assay of peripheral blood and hippocampal cells demonstrated no significant differences between caffeine-treated and control young adult mice in terms of DNA damage index (DI) and frequency. In contrast, when comparing young adult with aged animals, significant differences were observed in DNA damage in blood and hippocampal cells. The differences between aged animals (with or without caffeine) consisted of a significant decrease in DNA DI in the group that received caffeine. In the MN test, an increase in frequency of micronucleated polychromatic (PCE) erythrocytes was noted in aged animals that received water compared to young adult mice. In addition, comparing treated with control aged murine groups, a decrease in frequency of MN was found in PCE erythrocytes of caffeine-treated mice. Chronic caffeine consumption was neither genotoxic nor mutagenic at the dose tested; however, it appears that caffeine actually protected mice from genotoxicity and mutagenicity, consequences attributed to aging.
关于咖啡因摄入的研究表明,其与某些疾病的发展呈负相关,随后会出现有益的表现。我们的目的是评估咖啡因对年轻成年小鼠和老年小鼠外周血及神经组织DNA的影响。分别对雄性瑞士小鼠(年龄分别为2 - 3个月或16 - 18个月)用咖啡因溶液(0.3 g/l)处理4周,而对照组给予水。处理后,收集血液和海马细胞(用于彗星试验)以及股骨(用于微核[MN]试验)。外周血和海马细胞的彗星试验表明,在DNA损伤指数(DI)和频率方面,咖啡因处理组和对照组的年轻成年小鼠之间没有显著差异。相比之下,当比较年轻成年动物和老年动物时,在血液和海马细胞的DNA损伤方面观察到显著差异。老年动物(无论是否给予咖啡因)之间的差异在于接受咖啡因的组中DNA DI显著降低。在微核试验中,与年轻成年小鼠相比,接受水的老年动物中微核多染红细胞(PCE)的频率增加。此外,比较处理后的老年小鼠组和对照组,在咖啡因处理的小鼠的PCE红细胞中发现微核频率降低。在所测试的剂量下,长期摄入咖啡因既没有遗传毒性也没有致突变性;然而,似乎咖啡因实际上保护小鼠免受遗传毒性和致突变性的影响,这些影响归因于衰老。