Avaliação dos efeitos da cafeína na longevidade do nematódeo caenorhabditis elegans

Abstract

Caffeine is present in large amount of products consumed in the diet and it has been considered the most widely used psychoactive drug worldwide. In mammals, low doses of caffeine promote antagonism of adenosine receptors, mainly A1 and A2A. Studies in animal models suggest that caffeine may positive impact on development of neuropsychiatric diseases like Alzheimer, Parkinson, Huntington and chronic diseases (diabetes, inflammatory diseases and stroke). These pathologies are frequently associated to aging process which can be characterized by the organism progressive deterioration. The nematode Caenorhabditis elegans is a powerful model for aging studies, since it has experimental features which allow to explore the aging determinants. In the worm, aging is controlled by many factors, for instance, the insulin/IGF-1 pathway. Then, this study aimed to evaluate the effects of exposure to caffeine on the nematode Caenorhabditis elegans longevity and their determinants. It was observed that caffeine increased the lifespan following dose-dependent pattern. This effect is reliant on the exposure to this substance throughout the entire the animal life and it is mediated, in part, by insulin/IGF-1 activity. Furthermore, the exposition to caffeine delayed the larval development, reduced the number of offspring and the animals length. Interestingly, adenosine was able to reverse the increase on longevity promoted by caffeine and partially recovered the decrease of offspring. This fact suggests that, as observed in mammals, caffeine shares, if not the same, some molecular target from adenosine. The clarification of the mechanisms that the caffeine exposition outcome on the observed phenotypes can disclose new determinant genes from aging process. Moreover, due to the high world caffeine consumption, it becomes necessary to understand and even modulate the molecular targets aiming for higher longevity.