Purpose: The oxidative stress (OS) hypothesis of overtraining syndrome argues that increased production of free radicals through exercise cause muscle fatigue and damage resulting in lower athletic performance. Severa...Purpose: The oxidative stress (OS) hypothesis of overtraining syndrome argues that increased production of free radicals through exercise cause muscle fatigue and damage resulting in lower athletic performance. Several studies have investigated OS immediately before and after exercise bouts in a training macrocycle. Our study aimed to compare OS of endurance athletes between a competition macrocycle and the immediate post-season recovery macrocycle. In addition, we aimed to identify athletes who experienced an unexplainable drop in athletic performance during the competition season in order to compare their OS to those who experienced no drop in performance. Methods: Fifteen members of the University of Alaska Fairbanks cross country ski team volunteered for this study. Blood samples were taken in early February (“mid-season”) and late April (“post-season”). Participants completed questionnaires regarding physical activity and athletic performance at the time of the blood draws. Plasma was analyzed for 4-hydroxynonenal<sup> </sup>(HNE), nitrotyrosine,<sup> </sup>nitric oxide (NOX), and superoxide dismutase (SOD). Significance was determined by Wilcoxon and Mann-Whitney tests. Results: Participants displayed significantly higher (p Conclusion: Signs of oxidative stress and mitigation during the post-season recovery macrocycle were higher in athletes who reported experiencing a drop in athletic performance during the competition season macrocycle.展开更多
Noise-induced hearing loss is the primary non-genetic factor contributing to auditory dysfunction.However,there are currently no effective pharmacological interventions for patients with noise-induced hearing loss.Her...Noise-induced hearing loss is the primary non-genetic factor contributing to auditory dysfunction.However,there are currently no effective pharmacological interventions for patients with noise-induced hearing loss.Here,we present evidence suggesting that the lysine-specific demethylase 1 inhibitor–tranylcypromine is an otoprotective agent that could be used to treat noise-induced hearing loss,and elucidate its underlying regulatory mechanisms.We established a mouse model of permanent threshold shift hearing loss by exposing the mice to white broadband noise at a sound pressure level of 120 d B for 4 hours.We found that tranylcypromine treatment led to the upregulation of Sestrin2(SESN2)and activation of the autophagy markers light chain 3B and lysosome-associated membrane glycoprotein 1 in the cochleae of mice treated with tranylcypromine.The noise exposure group treated with tranylcypromine showed significantly lower average auditory brainstem response hearing thresholds at click,4,8,and 16 k Hz frequencies compared with the noise exposure group treated with saline.These findings indicate that tranylcypromine treatment resulted in increased SESN2,light chain 3B,and lysosome-associated membrane glycoprotein 1 expression after noise exposure,leading to a reduction in levels of 4-hydroxynonenal and cleaved caspase-3,thereby reducing noise-induced hair cell loss.Additionally,immunoblot analysis demonstrated that treatment with tranylcypromine upregulated SESN2 expression via the autophagy pathway.Tranylcypromine treatment also reduced the production of NOD-like receptor family pyrin domaincontaining 3(NLRP3)production.In conclusion,our results showed that tranylcypromine treatment ameliorated cochlear inflammation by promoting the expression of SESN2,which induced autophagy,thereby restricting NLRP3-related inflammasome signaling,alleviating cochlear hair cell loss,and protecting hearing function.These findings suggest that inhibiting lysine-specific demethylase 1 is a potential therapeutic strategy for preventing展开更多
Objective:The frequent consumption of deep-fried foods has been linked to high risk of certain non-communicable diseases.As a consequence,the safety of deep-fried oil(DFO)ingested with fried foods has been called into...Objective:The frequent consumption of deep-fried foods has been linked to high risk of certain non-communicable diseases.As a consequence,the safety of deep-fried oil(DFO)ingested with fried foods has been called into question.This study therefore evaluated the effects of DFO from palm kernel on serum 4-hydroxynonenal protein adduct formation,De Ritis ratio(DRR),liver histology and atherogenicity in Wistar rats and the role of vitamin C intervention.Methods:Deep-fried oil samples were characterized for total antioxidant capacity(TAC),degradation and metal contamination levels and compared against counterpart unused frying oil(UFO).In the animal experiment,both oil samples,sourced from commercial cooks,were orally administered,for 13 weeks,to sixty-two rats randomly divided into six test groups of two exposure levels alongside vitamin C control.After exposure,serum liver enzyme activities and lipoproteins levels were determined using colorimetric methods,while protein adducts levels were determined using enzyme-linked immunosorbent assay(ELISA).Histopathological examinations of liver tissues were also performed.Results:DFO had significantly lower(P=0.021)TAC,significantly higher(P=0.024)volatile acid and Pb concentrations compared to UFO.Exposure to DFO significantly increased(P<0.01)serum protein adduct formation,the De Ritis ratio and caused cytoplasmic vacuolation and pigment deposit on liver tissues compared to the control.Additionally,DFO exposures had an initial negative body weight gain rate that increased at the end of the study.Conclusion:However,co-administration of vitamin C significantly reduced(P<0.05)the De Ritis ratio and reduced the serum protein adducts levels by at least 15%.Concomitant intake of vitamin C and DFO can mitigate probable adverse effects.展开更多
文摘Purpose: The oxidative stress (OS) hypothesis of overtraining syndrome argues that increased production of free radicals through exercise cause muscle fatigue and damage resulting in lower athletic performance. Several studies have investigated OS immediately before and after exercise bouts in a training macrocycle. Our study aimed to compare OS of endurance athletes between a competition macrocycle and the immediate post-season recovery macrocycle. In addition, we aimed to identify athletes who experienced an unexplainable drop in athletic performance during the competition season in order to compare their OS to those who experienced no drop in performance. Methods: Fifteen members of the University of Alaska Fairbanks cross country ski team volunteered for this study. Blood samples were taken in early February (“mid-season”) and late April (“post-season”). Participants completed questionnaires regarding physical activity and athletic performance at the time of the blood draws. Plasma was analyzed for 4-hydroxynonenal<sup> </sup>(HNE), nitrotyrosine,<sup> </sup>nitric oxide (NOX), and superoxide dismutase (SOD). Significance was determined by Wilcoxon and Mann-Whitney tests. Results: Participants displayed significantly higher (p Conclusion: Signs of oxidative stress and mitigation during the post-season recovery macrocycle were higher in athletes who reported experiencing a drop in athletic performance during the competition season macrocycle.
基金supported by the National Key Research and Development Program of China,No.2022YFC2402701(to WC)Key International(Regional)Joint Research Program of the National Natural Science Foundation of China,No.81820108009(to SY)+5 种基金the National Natural Science Foundation of China,Nos.81970890(to WC)and 82371148(to WG)Fujian Provincial Healthcare Young and Middle-aged Backbone Talent Training Project,No.2023GGA035(to XC)Spring City Planthe High-level Talent Promotion and Training Project of Kunming,No.2022SCP001(to SY)the Natural Science Foundation of Hainan Province of China,No.824MS052(to XS)the Sixth Medical Center of Chinese PLA General Hospital Innovation Cultivation,No.CXPY202116(to LX)。
文摘Noise-induced hearing loss is the primary non-genetic factor contributing to auditory dysfunction.However,there are currently no effective pharmacological interventions for patients with noise-induced hearing loss.Here,we present evidence suggesting that the lysine-specific demethylase 1 inhibitor–tranylcypromine is an otoprotective agent that could be used to treat noise-induced hearing loss,and elucidate its underlying regulatory mechanisms.We established a mouse model of permanent threshold shift hearing loss by exposing the mice to white broadband noise at a sound pressure level of 120 d B for 4 hours.We found that tranylcypromine treatment led to the upregulation of Sestrin2(SESN2)and activation of the autophagy markers light chain 3B and lysosome-associated membrane glycoprotein 1 in the cochleae of mice treated with tranylcypromine.The noise exposure group treated with tranylcypromine showed significantly lower average auditory brainstem response hearing thresholds at click,4,8,and 16 k Hz frequencies compared with the noise exposure group treated with saline.These findings indicate that tranylcypromine treatment resulted in increased SESN2,light chain 3B,and lysosome-associated membrane glycoprotein 1 expression after noise exposure,leading to a reduction in levels of 4-hydroxynonenal and cleaved caspase-3,thereby reducing noise-induced hair cell loss.Additionally,immunoblot analysis demonstrated that treatment with tranylcypromine upregulated SESN2 expression via the autophagy pathway.Tranylcypromine treatment also reduced the production of NOD-like receptor family pyrin domaincontaining 3(NLRP3)production.In conclusion,our results showed that tranylcypromine treatment ameliorated cochlear inflammation by promoting the expression of SESN2,which induced autophagy,thereby restricting NLRP3-related inflammasome signaling,alleviating cochlear hair cell loss,and protecting hearing function.These findings suggest that inhibiting lysine-specific demethylase 1 is a potential therapeutic strategy for preventing
文摘目的初步探讨星形胶质细胞瘤细胞中的醛酮还原酶1A1(AKR1A1)在抗氧化应激和有毒醛代谢中的作用。方法通过LipofectamineTM RNAiMax以siRNA转染1321N1细胞,用Western blot法和qRT-PCR检测1321N1细胞中AKR1A1基因抑制水平。siRNA转染后的细胞经H2O2和4-羟基壬烯醛处理后使用MTT法检测细胞成活率;采用2',7'-二氯二氢荧光黄双乙酸酯(DCFH-DA)标记法检测敲减AKR1A1基因对H2O2诱导的1321N1细胞内活性氧(ROS)水平的影响。结果 Western blot法和qRT-PCR结果显示1321N1细胞经特异性siRNA转染后,AKR1A1基因的表达受到明显抑制(70%)。MTT法检测结果显示,siRNA-AKR1A1转染后的1321N1细胞在H2O2或4-羟基壬烯醛压力下的细胞成活率显著降低,而且敲减AKR1A1的1321细胞内H2O2诱导的ROS水平显著高于对照细胞。结论使用的特异性siRNA能有效抑制AKR1A1基因在1321N1星形细胞瘤细胞中表达,AKR1A1参与1321N1脑星形细胞瘤细胞中的4-羟基壬烯醛代谢,并且很可能参与调节脑细胞的抗氧化应激机制。
文摘Objective:The frequent consumption of deep-fried foods has been linked to high risk of certain non-communicable diseases.As a consequence,the safety of deep-fried oil(DFO)ingested with fried foods has been called into question.This study therefore evaluated the effects of DFO from palm kernel on serum 4-hydroxynonenal protein adduct formation,De Ritis ratio(DRR),liver histology and atherogenicity in Wistar rats and the role of vitamin C intervention.Methods:Deep-fried oil samples were characterized for total antioxidant capacity(TAC),degradation and metal contamination levels and compared against counterpart unused frying oil(UFO).In the animal experiment,both oil samples,sourced from commercial cooks,were orally administered,for 13 weeks,to sixty-two rats randomly divided into six test groups of two exposure levels alongside vitamin C control.After exposure,serum liver enzyme activities and lipoproteins levels were determined using colorimetric methods,while protein adducts levels were determined using enzyme-linked immunosorbent assay(ELISA).Histopathological examinations of liver tissues were also performed.Results:DFO had significantly lower(P=0.021)TAC,significantly higher(P=0.024)volatile acid and Pb concentrations compared to UFO.Exposure to DFO significantly increased(P<0.01)serum protein adduct formation,the De Ritis ratio and caused cytoplasmic vacuolation and pigment deposit on liver tissues compared to the control.Additionally,DFO exposures had an initial negative body weight gain rate that increased at the end of the study.Conclusion:However,co-administration of vitamin C significantly reduced(P<0.05)the De Ritis ratio and reduced the serum protein adducts levels by at least 15%.Concomitant intake of vitamin C and DFO can mitigate probable adverse effects.
