Regular and Moderate Exercise Counteracts the Decline of Antioxidant Protection but Not Methylglyoxal‐Dependent Glycative Burden in the Ovary of Reproductively Aging Mice

Abstract

Population aging results in urgent needs of interventions aimed at ensuring healthy senescence. Exercise often results in healthy aging, yet many molecular mechanisms underlying such effects still need to be identified. We here investigated whether the age-dependent accumulation of oxidative and methylglyoxal- (MG-) related molecular damage could be delayed by moderate exercise in the mouse ovary, an organ that first exhibits impaired function with advancing age in mammals. CD1 female mice underwent two- or four-month treadmill-based running through the transition from adult to middle age, when ovaries show signs of senescence, and markers of protection against reactive oxygen species (ROS) and MG were measured. The long-term exercise reduced the protein oxidative damage in the ovaries (P < 0.01), and this was linked to the preservation of the glutathione peroxidase protection against ROS (P < 0.001), as well as to the increased glutathione availability (P < 0.001). Conversely, even though the age-related deactivation of the MG-targeting systems was partially prevented by the long-term running programme (P < 0.001), exercised mice were not protected from the age-dependent glycative burden. In summary, lately initiated regular and moderate exercise limited some changes occurring in the ovaries of middle-aged mice, and this might help to develop nonpharmacological cointerventions to reduce the vulnerability of mammalian ovaries towards redox dysfunctions.

Power frequency magnetic field promotes a more malignant phenotype in neuroblastoma cells via redox-related mechanisms

“…As already reported 65 – 67 , the ratio of specific activities of coupled antioxidant enzymes is much better indicative of the efficiency of the antioxidative enzymatic defence than each activity alone. Statistically significant main effects of both MF exposure and time on the GPX/tSOD ratio were found (F = 186.1, P < 0.001 and F = 13.86, P < 0.01, respectively).…”

Oleuropein-Induced Apoptosis Is Mediated by Mitochondrial Glyoxalase 2 in NSCLC A549 Cells: A Mechanistic Inside and a Possible Novel Nonenzymatic Role for an Ancient Enzyme

“…One unit of activity was defined as 1 μ mol of S-D-lactoylglutathione produced min −1 . Conversely, Glo2 activity was assayed spectrophotometrically, at 25°C by recording the decrease in absorbance at 240 nm due to S-D-lactoylglutathione (0.3 mM) hydrolysis [21, 22]. One unit activity was defined as 1 μ mol S-D-lactoylglutathione hydrolyzed/min.…”

SIRT1-Dependent Upregulation of Antiglycative Defense in HUVECs Is Essential for Resveratrol Protection against High Glucose Stress

“…HG induced also an increase in GSSG/GSH ratio, which points to a pro-oxidant shift in the redox balance of glutathione. Upon redox stress, an important defense is provided by the enzymatic couple CAT/SOD, which ensures a rapid flux in the removal process of the redox couple O 2 − /H 2 O 2 [45,57,58]. Our assays revealed a prominent reduction in the CAT/SOD ratio upon HG, which is suggestive of an impairment of the O 2 − /H 2 O 2 detoxification process.…”

“…None of the three enzymes was modulated by HG at translational level ( p > 0.05, HG vs. CTR; Figure 5d–f). In addition, since the ratio of specific activities of coupled antioxidant enzymes much better reflects the status of the antioxidative enzymatic defense than each activity alone [57,58,59], we calculated the CAT/tSOD ratio, which is far more indicative of the overall ROS-targeting efficiency. Our data showed that HG strongly reduced the CAT over tSOD ratio, with respect to untreated cells ( p < 0.001, HG vs. CTR; Figure 5j).…”