AI Article Synopsis
- Aging and age-related diseases are linked to oxidative stress and inflammation, prompting research into nonsteroidal anti-inflammatory drugs (NSAIDs) for potential lifespan extension.
- In a study with Caenorhabditis elegans, aspirin and ibuprofen were found to extend lifespan in both young and old worms by reducing reactive oxygen species (ROS) and boosting antioxidant gene expression.
- Conversely, acetaminophen and indomethacin worsened aging in older worms, suggesting they may pose risks rather than benefits for elderly individuals due to increased toxicity and oxidative stress.
Article Abstract
Aging and age-related diseases are intricately associated with oxidative stress and inflammation. Nonsteroidal anti-inflammatory drugs (NSAIDs) have shown their promise in mitigating age-related conditions and potentially extending lifespan in various model organisms. However, the efficacy of NSAIDs in older individuals may be influenced by age-related changes in drug metabolism and tolerance, which could result in age-dependent toxicities. This study aimed to evaluate the potential risks of toxicities associated with commonly used NSAIDs (aspirin, ibuprofen, acetaminophen, and indomethacin) on lifespan, healthspan, and oxidative stress levels in both young and old Caenorhabditis elegans. The results revealed that aspirin and ibuprofen were able to extend lifespan in both young and old worms by suppressing ROS generation and enhancing the expression of antioxidant SOD genes. In contrast, acetaminophen and indomeacin accelerated aging process in old worms, leading to oxidative stress damage and reduced resistance to heat stress through the pmk-1/skn-1 pathway. Notably, the harmful effects of acetaminophen and indomeacin were mitigated when pmk-1 was knocked out in the pmk-1(km25) strain. These results underscore the potential lack of benefit from acetaminophen and indomeacin in elderly individuals due to their increased susceptibility to toxicity. Further research is essential to elucidate the underlying mechanisms driving these age-dependent responses and to evaluate the potential risks associated with NSAID use in the elderly population.
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| http://dx.doi.org/10.1002/jat.4655 | DOI Listing |
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