scholarly journals Antioxidants Supplementation and Exercise Performance

2001 ◽  
Vol 7 (1) ◽  
pp. 61-65
Author(s):  
Andy C. M. LOK ◽  
Stephen H. S. WONG

LANGUAGE NOTE | Document text in English; abstract also in Chinese.Physical exercise is known to have many beneficial effects. However, intense physical training can concomitantly result in increased free radical production in human body, thereby inducing a greater oxidative-stress that may cause damage to the cells. In this article, the mechanism of free radicals formation, the assessment of oxidative stress in human, and the defense system in the body against the anti-oxidative damage will be discussed. Studies in the effect of antioxidant supplementation on exercise performance will also be reviewed. Research findings suggest that supplementation of antioxidants can reduce the oxidative damage to muscle and other tissues induced by vigorous exercise. However, the effect of such supplementation on exercise performance remains unclear.雖然運動對人體所產生的益處已被廣泛肯定,可是高強度的運動訓練卻會增加體內自由基的濃度,從而損害身體的組織。本文綜述自由基形成的機制,身體對自由基的反應,與及如何量度自由基對身體的損害和補充抗氧化劑對運動能力的影響。研究證實補充抗氧化劑能有效減低身體受自由基的傷害,但能否增進運動能力則尚需探究。

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
R. C. Patra ◽  
Amiya K. Rautray ◽  
D. Swarup

Oxidative stress has been implicated to play a role, at least in part, in pathogenesis of many disease conditions and toxicities in animals. Overproduction of reactive oxygen species and free radicals beyond the cells intrinsic capacity to neutralize following xenobiotics exposure leads to a state of oxidative stress and resultant damages of lipids, protein, and DNA. Lead and cadmium are the common environmental heavy metal pollutants and have widespread distribution. Both natural and anthropogenic sources including mining, smelting, and other industrial processes are responsible for human and animal exposure. These pollutants, many a times, are copollutants leading to concurrent exposure to living beings and resultant synergistic deleterious health effects. Several mechanisms have been explained for the damaging effects on the body system. Of late, oxidative stress has been implicated in the pathogenesis of the lead- and cadmium-induced pathotoxicity. Several ameliorative measures to counteract the oxidative damage to the body system aftermath or during exposure to these toxicants have been assessed with the use of antioxidants. The present review focuses on mechanism of lead- and cadmium-induced oxidate damages and the ameliorative measures to counteract the oxidative damage and pathotoxicity with the use of supplemented antioxidants for their beneficial effects.


Metabolism ◽  
2003 ◽  
Vol 52 (5) ◽  
pp. 586-589 ◽  
Author(s):  
D. Bonnefont-Rousselot ◽  
B. Raji ◽  
S. Walrand ◽  
M. Gardès-Albert ◽  
D. Jore ◽  
...  

Author(s):  
Krishna Reddy BV ◽  
Avinash Kumar Reddy G ◽  
Sujitha V ◽  
Manasa A

DM otherwise diabetes is now a days an epidemic with the percentage of patient population rising to almost 10% of the world population. Out of all the DM complications, cataract leads the way contributing to disabilities to about 60% of diabetic population. But the pathogenesis of DM cataract is still a half-understood area of medicine there by posing a problem in the therapy. The data that we have till now gives us enough evidence to advocate the oxidative stress has a major role for the pathogenesis of DM complications like DMnephropathy, DMneuropathy, and cardiac hypertrophy, which suggests the oxidative stress is a central feature of diabetes. In the current research, the pharmacological evaluation of Fisetin for its DM based anti-cataract property was performed. This research concentrates to estimate the possible involvement of Nrf-2 / heme oxygenase (HO)-pathway in the observed therapeutic effect, if any. The data obtained in this study also indicate that the observed beneficial effects mainly due to activation of Nrf2/HO-1 pathway. These effects probably result in increased tissue anti-oxidant status as well as decreased free radical production, which ultimately responsible for the observed beneficial effects of Fisetin against hyperglycemia-induced cataract.


2020 ◽  
Vol 24 (1) ◽  
pp. 39-44
Author(s):  
E. V. Smirnova ◽  
E. V. Proskurnina ◽  
T. N. Krasnova

BACKGROUND. Oxidative status impairment plays a significant role in the pathogenesis of SLE and lupus nephritis (LN). The data about oxidative status in this disease are incomplete, that’s why it’s necessary to use a new approach to study it. THE AIM: To study oxidative status in SLE patients with kidney involvement. PATIENTS AND METHODS:53 patients with SLE were included in this prospective study, among them 40 patients with different severity of kidney involvement, control group were 87 healthy donors. Oxidative stress parameters were measured: antioxidant activity (AOA) of blood plasma and parameters, characterizing the state of the main source of reactive oxygen species (ROS) – neutrophils, more specifically: specific spontaneous neutrophil activity, specific stimulated activity (peak and integral), coefficient of respiratory burst attenuation, representing the rate of free radical production decrease after stimulation, the higher the value of this parameter, the slower is free radical production decrease. RESULTS. It was shown elevation of neutrophil free radical-producing activity parameters and elevation of blood plasma AOA in patients with LN, comparing to healthy controls. Immunosuppressive therapy with glucocorticosteroids (GCS) and cytostatics (CS) increased blood plasma AOA comparing to monotherapy with GCS. A correlation between oxidative status impairment and intensity of inflammatory reactions was found: correlation of respiratory burst attenuation coefficient with blood sedimentation rate was shown. Reduction of spontaneous free radical-producing neutrophil activity was found in LN patients with NS, which might be the result of neutrophil functional activity attenuation in high disease activity. CONCLUSION. The increased free radical-producing neutrophil activity was shown, which might be the cause of oxidative stress in SLE with LN. It seems warranted investigation of these parameters in samples of larger volume to search targets aimed at neutrophils. The necessity of antioxidant therapy in patients with SLE seems doubtful, as they show significant increase of blood plasma AOA, which might result from compensatory reaction of human organism to oxidative stress and therapy with GCS and CS.


2015 ◽  
Vol 36 (6) ◽  
pp. 2217-2228 ◽  
Author(s):  
Xu Zha ◽  
Guojiu Wu ◽  
Xueying Zhao ◽  
Liqiong Zhou ◽  
Hong Zhang ◽  
...  

Background/Aims: Oxidative stress that damages cells of the retinal pigment epithelium (RPE) can cause the development of hereditary retinal disease (HRD). PRDX6, which is a member of the PRDX family, is essential for removing metabolic free radicals from the body. However, the effect of PRDX6 on oxidative stress in HRD remains unknown. In this study, we sought to investigate the role of PRDX6 in oxidative stress-induced HRD in ARPE-19 cells and the molecular mechanism involved. Methods: ARPE-19 cells were used in the current study. Intracellular ROS levels were determined by flow cytometry. Lipid peroxidation was measured using a commercial MDA assay kit. Cellular variability was determined by MTT assay. Apoptosis was determined using an Annexin V-FITC Apoptosis Detection Kit. mRNA and protein expression levels were detected by real-time PCR and western blot analysis, respectively. Results: We found that H2O2 and blue light could induce significant oxidative stress damage and cell death in ARPE-19 cells. Furthermore, we found that PRDX6 levels significantly decreased after H2O2 treatment. PRDX6 overexpression protected ARPE-19 cells from H2O2- and blue light-induced oxidative damage, while PRDX6 knockdown enhanced oxidative damage in these cells. Mechanistically, we found that PRDX6 prevented oxidative damage and promoted ARPE-19 cell survival through the PI3K/AKT signaling pathway. Conclusions: Collectively, these results suggest that PRDX6 protects ARPE-19 cells from H2O2-induced oxidative stress and apoptosis and that this protection is mediated at least partially through the PI3K/AKT pathway.


2016 ◽  
Vol 36 (5) ◽  
pp. 483-493 ◽  
Author(s):  
AO Abolaji ◽  
IO Awogbindin ◽  
IA Adedara ◽  
EO Farombi

The fungicide carbendazim (CBZ) and insecticide chlorpyrifos (CPF) are currently applied together by farmers for the control of pests. Here, we investigated the impacts of 7 days oral co-exposure to 10 mg/kg body weight of CPF and 50 mg/kg body weight of CBZ on selected oxidative stress and antioxidant biomarkers in the liver, kidney, and spleen of female rats. The results showed that while the body weight gain and relative organ weights were not significantly affected after separate exposure to CPF and CBZ, there was a significant decrease in the body weight gain with concomitant increases in the relative kidney and spleen weights of rats treated with the mixture. Also, CPF and CBZ co-exposure significantly increased the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea, and creatinine ( p < 0.05) when compared with the groups treated with CBZ or CPF alone and the control. The significant decreases in both antioxidant enzymes activities and nonenzymatic antioxidant level following individual administration of CPF and CBZ to rats were intensified in the co-exposure group ( p < 0.05). Additionally, the marked increases in the levels of oxidative stress indices in liver, kidney, and spleen of rats treated with CPF or CBZ alone were intensified in the co-exposure group ( p < 0.05). Histopathologically, co-exposure to CPF and CBZ exacerbates their individual effects on the liver, kidney, and spleen. These findings showed that co-exposure to CPF and CBZ in rats elicited more severe oxidative damage on the liver, kidney, and spleen of the rats, indicative of an additive effect compared to CPF or CBZ alone and as such, may pose a greater environmental risk to humans.


1994 ◽  
Vol 63 (1) ◽  
pp. 37-122 ◽  
Author(s):  
Mario E. Götz ◽  
Gabriella Künig ◽  
Peter Riederer ◽  
Moussa B.H. Youdim

2008 ◽  
Vol 59 (9) ◽  
Author(s):  
Mirela Ahmadi ◽  
Mihaela Pup ◽  
Lucia Olariu ◽  
Horia Vermesan ◽  
Radu Prejbeanu

The study presents the effect of Zn and Mn overdoses in relation with other trace metals in rat�s liver. All studied metals are involved in some enzymes activity, which are implicated in antioxidant defense system of the body. But, in some conditions � our case in overdoses � an imbalance can appear, and antioxidant character of a metal can become prooxidant. In this case, antagonistic or synergic behaviour in relation with other trace metals is obvious. The observed modifications are the increasing of zinc and manganese level in liver after solutions administration, and the amplification effect over the hepatic iron, with the possibility of oxidative stress appearance.


2018 ◽  
Vol 69 (7) ◽  
pp. 1616-1620
Author(s):  
Viviana Mihaela Ivan ◽  
Marius Georgescu ◽  
Adrian Apostol ◽  
Nicolae Albulescu ◽  
Alina Florina Serb ◽  
...  

Metabolic therapy constitutes a relatively new therapeutic option for ischemic heart disease (IHD). Metabolic agents including Trimetazidine [1-(2,3,4-trimethoxybenzyl) piperazine] (TMZ) are currently used as anti-ischemic cardiac drugs to alleviate this internal metabolic disturbance. The present study focused on the assessment of the beneficial effects of TMZ as additional medication to the conventional medical therapy in patients with myocardial infarction. The obtained results showed an increase of superoxide dismutase (SOD) activities and a faster normalization of total sialic acid (TSA) levels in patients with TMZ add-on therapy, in comparison to the control group, indicating a stabilization of the ischemic process under TMZ therapy, with decreased free radical production and restoration of the antioxidant capacity and of the membrane lesions. The present findings emphasize the importance of TMZ administration to prevent reperfusion-mediated cardiac injury and dysfunction and demonstrate that this promising therapeutic approach is worthy of further research.


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