Antioxidant defenses and lipid peroxidation during anoxia stress and aerobic recovery in the marine gastropod Littorina littorea

1998 ◽  
Vol 221 (2) ◽  
pp. 277-292 ◽  
Author(s):  
Tina M Pannunzio ◽  
Kenneth B Storey
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Defenses ◽  
Littorina Littorea ◽  
Marine Gastropod ◽  
Anoxia Stress

Short-term exercise training can improve myocardial tolerance to I/R without elevation in heat shock proteins

2001 ◽  
Vol 281 (3) ◽  
pp. H1346-H1352 ◽  
Author(s):  
Karyn L. Hamilton ◽  
Scott K. Powers ◽  
Takao Sugiura ◽  
Sunjoo Kim ◽  
Shannon Lennon ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Antioxidant Defenses ◽  
Control Group ◽  
Shock Proteins ◽  
Mnsod Activity ◽  
Over Time

We examined the effects of 3 days of exercise in a cold environment on the expression of left ventricular (LV) heat shock proteins (HSPs) and contractile performance during in vivo ischemia-reperfusion (I/R). Sprague-Dawley rats were divided into the following three groups ( n = 12/group): 1) control, 2) exercise (60 min/day) at 4°C (E-Cold), and 3) exercise (60 min/day) at 25°C (E-Warm). Left anterior descending coronary occlusion was maintained for 20 min, followed by 30 min of reperfusion. Compared with the control group, both the E-Cold and E-Warm groups maintained higher ( P < 0.05) LV developed pressure, first derivative of pressure development over time (+dP/d t), and pressure relaxation over time (−dP/d t) throughout I/R. Relative levels of HSP90, HSP72, and HSP40 were higher ( P < 0.05) in E-Warm animals compared with both control and E-Cold. HSP10, HSP60, and HSP73 did not differ between groups. Exercise increased manganese superoxide dismutase (MnSOD) activity in both E-Warm and E-Cold hearts ( P < 0.05). Protection against I/R-induced lipid peroxidation in the LV paralleled the increase in MnSOD activity whereas lower levels of lipid peroxidation were observed in both E-Warm and E-Cold groups compared with control. We conclude that exercise-induced myocardial protection against a moderate duration I/R insult is not dependent on increases in myocardial HSPs. We postulate that exercise-associated cardioprotection may depend, in part, on increases in myocardial antioxidant defenses.

Lipid peroxidation and antielastase activity in the lung under oxidant stress: role of antioxidant defenses

1991 ◽  
Vol 70 (4) ◽  
pp. 1456-1462 ◽  
Author(s):  
V. Mohsenin
Keyword(s):  
Lipid Peroxidation ◽  
Oxidant Stress ◽  
Lavage Fluid ◽  
Conjugated Dienes ◽  
Antioxidant Defenses ◽  
Vitamin Supplementation ◽  
Control Group ◽  
Early Event ◽  
Lipid Peroxidation Products

The role of lipid peroxidation in the inactivation of alpha 1-protease inhibitor (alpha 1-PI) in the alveolar lining fluid of human subjects has been examined under oxidant stress. Exposure to nitrogen dioxide (NO2) at 4 ppm for 3 h resulted in a significant increase in the amount of lipid peroxidation products in the alveolar lining fluid, with conjugated dienes the predominant species. Four-week supplementation with vitamins C and E before NO2 exposure markedly decreased the levels of conjugated dienes (control 804 +/- 103 pmol/micrograms total phospholipids vs. vitamin-supplemented 369 +/- 58, P = 0.003). Malondialdehydes, although detectable in the lavage fluid, contributed little to the total amount of lipid peroxidation products, and the levels were comparable in both groups. NO2 exposure in the absence of vitamin supplementation caused a significant decrease in the elastase inhibitory capacity (EIC) of the alveolar lining fluid in the control group but not in the vitamin-supplemented group [control 3.67 +/- 0.32 micrograms alpha 1-PI/micrograms porcine pancreatic elastase (PPE) vs. vitamin-supplemented 2.75 +/- 0.17, P less than 0.03]. The vitamin-supplemented group had a lower level of conjugated dienes and a higher EIC. Conversely, the control group had higher levels of conjugated dienes and a lower EIC in their lavage fluid. These studies demonstrate that lipid peroxidation occurs as an early event during oxidant exposure in the lungs of normal subjects. The appearance of lipid peroxidation products in the lavage fluid is associated with a decrease in the EIC of the alveolar lining fluid. Vitamins C and E diminish lipid peroxidation and preserve the EIC of the lower respiratory tract fluid during oxidant stress.

Lipid Peroxidation and Antioxidant Defenses in Cystic Fibrosis Patients

1999 ◽  
Vol 37 (5) ◽  
Author(s):  
Hassiba Benabdeslam ◽  
Hassane Abidi ◽  
Isabelle Garcia ◽  
Gabriel Bellon ◽  
Robert Gilly ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Lipid Peroxidation ◽  
Antioxidant Defenses

Antioxidant defenses and lipid peroxidation in the cerebral cortex and hippocampus following acute exposure to malathion and/or zinc chloride

Toxicology ◽  
2005 ◽  
Vol 207 (2) ◽  
pp. 283-291 ◽  
Author(s):  
Patrícia S. Brocardo ◽  
Pablo Pandolfo ◽  
Reinaldo N. Takahashi ◽  
Ana Lúcia S. Rodrigues ◽  
Alcir L. Dafre
Keyword(s):  
Lipid Peroxidation ◽  
Cerebral Cortex ◽  
Zinc Chloride ◽  
Acute Exposure ◽  
Antioxidant Defenses

scholarly journals Oxidative stress in dogs

2016 ◽  
Vol 37 (3) ◽  
pp. 1431 ◽  
Author(s):  
Claudia Russo ◽  
Ana Paula F. Rodrigues Loureiro Bracarense
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Free Radicals ◽  
Cell Membrane ◽  
The Body ◽  
Antioxidant Defenses ◽  
Cellular Respiration ◽  
Bodily Fluids ◽  
Cellular Components ◽  
Harmful Effects

Reactive oxygen species (ROS), also known as free radicals, are generated during cellular respiration. Under normal conditions, the body has the ability to neutralize the effects of free radicals by using its antioxidant defenses. In the case of an imbalance between oxidants and antioxidants, free radical production exceeds the capacity of organic combustion, resulting in oxidative stress. Of all the cellular components compromised by the harmful effects of ROS, the cell membrane is the most severely affected owing to lipid peroxidation, which invariably leads to changes in the membrane structure and permeability. With lipid peroxidation of the cell membrane, some by-products can be detected and measured in tissues, blood, and other bodily fluids. The measurement of biomarkers of oxidative stress is commonly used to quantify lipid peroxidation of the cell membrane in humans, a species in which ROS can be considered as a cause or consequence of oxidative stress-related diseases. In dogs, few studies have demonstrated this correlation. The present review aims to identify current literature knowledge relating to oxidative stress diseases and their detection in dogs.

scholarly journals Oxidative stress and antioxidant defenses in mild cognitive impairment: a systematic review and meta-analysis.

2021 ◽  
Author(s):  
gallayaporn nantachai ◽  
Asara Vasupanrajit ◽  
Chavit Tunvirachaisakul ◽  
Marco Solmi ◽  
Michael Maes
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Web Of Science ◽  
Reduced Glutathione ◽  
Meta Analysis ◽  
Antioxidant Defenses ◽  
Healthy Controls ◽  
Standardized Mean Difference

This study aims to systematically review and meta-analyze the nitro-oxidative stress (O&NS)/antioxidant (ANTIOX) ratio in the peripheral blood of people with mild cognitive impairment (MCI). We searched PubMed, Scopus, Google Scholar, and Web of Science for articles published from inception until July 31, 2021. Forty-six studies on 3.798 MCI individuals and 6.063 healthy controls were included. The O&NS/ANTIOX ratio was significantly higher in MCI than in controls with a Standardized Mean Difference (SMD)=0.378 (95% CI: 0.250; 0.506). MCI individuals showed increased lipid peroxidation (SMD=0.774, 95%CI: 4.416; 1.132) and O&NS-associated toxicity (SMD=0.621, CI: 0.377; 0.865) and reduced glutathione (GSH) defenses (SMD=0.725, 95%CI: 0.269; 1.182) as compared with controls. MCI was also accompanied by significantly increased homocysteine (SMD=0.320, CI: 0.059; 0.581), but not protein oxidation, and lowered non-vitamin (SMD=0.347, CI: 0.168; 0.527) and vitamin (SMD=0.564, CI: 0.129; 0.999) antioxidant defenses. The results show that MCI is at least in part due to increased neuro-oxidative toxicity and suggest that treatments targeting lipid peroxidation and the GSH system may be used to treat or prevent MCI.

scholarly journals Oxidative Stress and Antioxidant Defenses in Mild Cognitive Impairment: A Systematic Review and Meta-Analysis

2021 ◽  
Author(s):  
Gallayaporn Nantachai ◽  
Asara Vasupanrajit ◽  
Chavit Tunvirachaisakul ◽  
Marco Solmi ◽  
Michael Maes Michael Maes
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Web Of Science ◽  
Reduced Glutathione ◽  
Meta Analysis ◽  
Antioxidant Defenses ◽  
Healthy Controls ◽  
Standardized Mean Difference

This study aims to systematically review and meta-analyze the nitro-oxidative stress (O&amp;NS)/antioxidant (ANTIOX) ratio in the peripheral blood of people with mild cognitive impairment (MCI). We searched PubMed, Scopus, Google Scholar, and Web of Science for articles published from inception until July 31, 2021. Forty-six studies on 3.798 MCI individuals and 6.063 healthy controls were included. The O&amp;NS/ANTIOX ratio was significantly higher in MCI than in controls with a Standardized Mean Difference (SMD)=0.378 (95% CI: 0.250; 0.506). MCI individuals showed increased lipid peroxidation (SMD=0.774, 95%CI: 4.416; 1.132) and O&amp;NS-associated toxicity (SMD=0.621, CI: 0.377; 0.865) and reduced glutathione (GSH) defenses (SMD=0.725, 95%CI: 0.269; 1.182) as compared with controls. MCI was also accompanied by significantly increased homocysteine (SMD=0.320, CI: 0.059; 0.581), but not protein oxidation, and lowered non-vitamin (SMD=0.347, CI: 0.168; 0.527) and vitamin (SMD=0.564, CI: 0.129; 0.999) antioxidant defenses. The results show that MCI is at least in part due to increased neuro-oxidative toxicity and suggest that treatments targeting lipid peroxidation and the GSH system may be used to treat or prevent MCI.

Relationship between anoxia exposure and antioxidant status in the frog Rana pipiens

1996 ◽  
Vol 271 (4) ◽  
pp. R918-R925 ◽  
Author(s):  
M. Hermes-Lima ◽  
K. B. Storey
Keyword(s):  
Skeletal Muscle ◽  
Lipid Peroxidation ◽  
Rana Pipiens ◽  
Thiobarbituric Acid ◽  
Leopard Frog ◽  
Antioxidant Defenses ◽  
Glutathione S Transferase ◽  
Glutathione Status ◽  
Organ Specific

The biochemical adaptations of cellular antioxidant defenses that permit anoxia-tolerant animals to deal effectively with rapid and large changes in oxygen availability, and hence oxidative stress, during transitions from anoxia to normoxia provide insights into the strategies of antioxidant defense that could help to minimize reperfusion injuries to mammalian organs after anoxia/ischemia stress. The present study analyzes the effects of 30 h anoxia exposure followed by reoxygenation on the antioxidant defenses (activities of five enzymes, glutathione status) and lipid peroxidation damage to organs of the leopard frog Rana pipiens (5 degrees C-adapted autumn frogs). Exposure to 30 h anoxia resulted in significant increases in the activities of skeletal muscle and heart catalase (by 53 and 47%), heart and brain glutathione peroxidase (by 75 and 30%), and brain glutathione S-transferase (by 66%). In most cases, enzyme activities had returned to the control values after 40 h aerobic recovery. Activities of superoxide dismutase and glutathione reductase were unaltered in all of the organs, and anoxia/recovery had no effect on any of the enzymes in liver. Glutathione equivalents (GSH-eq) were maintained in four organs during anoxia but decreased by 32% in brain during anoxia. Brain GSH-eq had recovered after 90 min reoxygenation, and, in addition, hepatic GSH-eq rose by 71% after 90 min reoxygenation. The ratio of oxidized glutathione to GSH-eq was also affected by anoxia in an organ-specific way. Lipid peroxidation, assessed as the content of thiobarbituric acid-reactive substances (TBARS), was unaltered in skeletal muscle and liver after 30 h anoxia exposure or short (25 and 90 min)- or long-term (40 h) periods of reoxygenation, indicating that cycles of natural and survivable anoxia/reoxygenation occur without significant increase in TBARS in selected organs. Overall, the data demonstrate that elements of the antioxidant system of R. pipiens are induced during anoxia exposures as a possible preparation for dealing with potentially harmful oxygen reperfusion stress.

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