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Hearing loss resulting from overexposure to entertainment-related sounds is a modern concern. "Epic Ear Defence" places the player in the three-dimensional environment of the ear canal and challenges the player to defend the ear from various noises, to delay the onset of noise-related hearing loss.

High levels of homocysteine (Hcy) accelerate endothelial cell damage by producing hydrogen peroxide (H(2)O(2)). We investigated whether 17-beta estradiol may prevent the accelerated rate of endothelial cell detachment and reduced cell viability in cultured endothelial cells challenged with Hcy. Cultured bovine aortic endothelial cells (BAEC) were incubated for 72-h with either vehicle (alcohol) or different concentrations of 17-beta estradiol (1 nM [1E2] and 10 nM [10E2]) before being challenged with 0.5 mM of Hcy. Cell viability and H(2)O(2) levels were evaluated at 30 min, 1-, 2-, 4-, 8-, and 24-h after adding Hcy. Cell suspensions were frozen in liquid nitrogen and used later for spectrophotometric measurement of intracellular glutathione (GSH) levels. Cell viability 24 h after Hcy administration was significantly lower in vehicle versus 1 nM and 10 nM 17-beta estradiol (44 +/- 5% vs. 70.66 +/- 4%, [p < 0.001] and 79 +/- 5% respectively, [p < 0.001]). H(2)O(2) levels were higher in vehicle (1 +/- 0.05 microM) compared with 1E2 and 10E2 (0.8 +/- 0.1 microM, p = 0.02 and 0.1 +/- 0.05 microM, respectively, p < 0.001), whereas GSH content was increased in 1E1 and 10E2 versus control (27.69 +/- 4.6 nM/10(6) cells and 43.49 +/- 5.5 nM/10(6) cells vs. 13.33 +/- 1.5 nM/10(6) cells, p < 0.001). Bovine aortic endothelial cells treatment with 17-beta estradiol (0, 1, and 10 nM) and 0.1 mmol buthionine sulfoximine, an inhibitor of gamma-glutamylcysteine synthase, abolished the beneficial effects of estradiol alone on cell viability, GSH content, and H2O2 generation. Estradiol prevents Hcy-induced endothelial cell injury by increasing the intracellular content of GSH.

Objective: We investigated whether estradiol may prevent accelerated atherosclerosis due to hyperhomocysteinemia by enhancing the antioxidant system., Methods: Male Wistar rats were treated with placebo (P) or 1 mg (1E2) and 2 mg (2E2) 17 beta estradiol. Half of the animals (n=6) from each group received homocysteine (Hcy, 100 mg/kg/day) administered in the drinking water for 60 days (P/Hcy, 1E2/Hcy and 2E2/Hcy). Glutathione (GSH) content and glucose-6-phosphate dehydrogenase (G6PDH) activity were determined in myocardial tissues, as well as the serum Hcy concentrations and blood levels of hydrogen peroxide (H(2)O(2)). The relaxation response of aortic ring segments to acetylcholine (ACh) was used for the assessment of endothelial function, and hematoxylin-eosin stained thin sections of rat aorta were used for detection of the histological changes (namely endothelial damage and wall thickening)., Results: Depression of relaxation to ACh occurred in P/Hcy compared to P (15.7 +/- 4% vs. 96.3 +/- 7%, P<0.0001), but estrogen significantly restored endothelium dependent relaxation in hyperhomocysteinemic rats (86.8 +/- 9.3%, P<0.001). Histological examination revealed aortic endothelial denudation in P/Hcy while the endothelial structures of the aorta from the 1E2/Hcy and 2E2/Hcy appeared normal. Significant reductions in GSH and G6PDH levels were detected in P/Hcy (1.5 +/- 0.01 micromol/g and 3.21 +/- 1.2 U/mg, respectively) compared to 1E2/Hcy (2.5 +/- 0.3 micromol/g and 12.81 +/- 1.5 U/mg, P<0.001) and 2E2/Hcy (3.11 +/- 1.1 micromol/g and 15.66 +/- 4 U/mg, P<0.001). In addition, blood H(2)O(2) level in 1E2/Hcy and 2E2/Hcy remained low while it was raised significantly in P/Hcy compared to P (P<0.001)., Conclusions: These data suggest that the observed reduction of GSH levels and suppression of G6PDH activity induced by Hcy coupled, with endothelial ultrastructural changes and impaired function, all reversed by estradiol, may have relevance to the mechanisms of atherogenesis and the beneficial effects of estrogen replacement therapy.