The aged-related increase in xanthine oxidase expression and activity in several tissues from mice is not shown in long-lived animals

Abstract

Xanthine oxidase (XO) is an important source of oxidant production and plays an essential role in several oxidative stress-related diseases. Aging is associated with a progressive deregulation of homeostasis as a result of a chronic oxidative stress situation. In the present work the age-related changes in XO expression and activity, as well as the activities of superoxide dismutase and catalase have been investigated in liver, kidney and thymus from four different age groups of mice, including long-lived animals. Furthermore, we have evaluated the contribution of the XO to the oxidative stress-associated with aging, in comparison to another enzymatic key source of oxidant generation, the NADPH oxidase, in peritoneal leukocytes from old mice. In all the tissues analyzed, the old mice showed higher activity and expression of XO, and decreased or unchanged superoxide dismutase and catalase activities as compared with adult mice. Moreover, the inhibition of reactive oxygen species with allopurinol or apocynin in peritoneal leukocytes from old mice, suggest that both XO and NADPH oxidase contribute to the generation of superoxide anion, whereas the XO may have a special relevance in the production of hydrogen peroxyde. Finally, long-lived animals showed a well-preserved redox state, in terms of antioxidant defenses and oxidant compounds in tissues and immune cells, which may be related to the ability of these subjects to reach a very advanced age in healthy condition. These results confirm that XO plays an important role in the age-related oxidative stress in tissues and immune cells.

Thin endometrium transcriptome analysis reveals a potential mechanism of implantation failure

“…These genes have essential roles in the response to oxidative stress 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25…”

“…The activation of PPAR‐ γ is an important factor in the protection against oxidative stress in cells, such as vascular endothelial cells and cardiomyocytes 16, 17, 20, 21, 24, 25. Xanthine dehydrogenase reduces age‐related oxidative stress in tissues and immune cells 23. Carbonyl reductase 3 is regulated via NRF2 ‐dependent signaling pathways and helps to alleviate oxidative stress 18.…”

Oxidative Stress and Anti-Oxidant Enzyme Activities in the Trophocytes and Fat Cells of Queen Honeybees (Apis mellifera)

“…32,37 Therefore, the higher levels of ROS in old queens may be due to higher energy metabolism, which increases the production of superoxide and other ROS. 6 Although XO activity increased with aging in human plasma, rat plasma, rat aorta, rat gastrocnemius muscle, mice cerebral cortex, mice liver, mice plasma, mice spleen, and mice thymus, [38][39][40] XO activity did not change with aging in mice kidney, mice lung, long-lived mice liver, long-lived mice kidney, and long-lived mice plasma. 39,40 In this study, XO activity is not significantly different between young and old queens.…”

“…6 Although XO activity increased with aging in human plasma, rat plasma, rat aorta, rat gastrocnemius muscle, mice cerebral cortex, mice liver, mice plasma, mice spleen, and mice thymus, [38][39][40] XO activity did not change with aging in mice kidney, mice lung, long-lived mice liver, long-lived mice kidney, and long-lived mice plasma. 39,40 In this study, XO activity is not significantly different between young and old queens. This phenomenon is consistent with a previous study, showing that XO activity is not significantly different between young and long-lived mice.…”

“…This phenomenon is consistent with a previous study, showing that XO activity is not significantly different between young and long-lived mice. 40 The explanation is most likely that XO does not participate in the impairment of trophocytes and fat cells with aging in queens. This inference is in agreement with a previous study showing that XO does not contribute to impaired peripheral conduit artery endothelium-dependent dilatation with aging in human.…”