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

Intracerebroventricular administration of N-acetylaspartic acid impairs antioxidant defenses and promotes protein oxidation in cerebral cortex of rats

2009 ◽  
Vol 24 (2) ◽  
pp. 283-298 ◽  
Author(s):  
Carolina Didonet Pederzolli ◽  
Francieli Juliana Rockenbach ◽  
Fernanda Rech Zanin ◽  
Nicoli Taiana Henn ◽  
Eline Coan Romagna ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Protein Oxidation ◽  
Antioxidant Defenses ◽  
Intracerebroventricular Administration

Increased in vitro lipid peroxidation of gerbil cerebral cortex as compared with rat

1986 ◽  
Vol 67 (1) ◽  
pp. 63-67 ◽  
Author(s):  
Joyce A. DeLeo ◽  
Robert A. Floyd ◽  
John M. Carney
Keyword(s):  
Lipid Peroxidation ◽  
Cerebral Cortex

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.

Acute administration of 5-oxoproline induces oxidative damage to lipids and proteins and impairs antioxidant defenses in cerebral cortex and cerebellum of young rats

2010 ◽  
Vol 25 (2) ◽  
pp. 145-154 ◽  
Author(s):  
Carolina Didonet Pederzolli ◽  
Caroline Paula Mescka ◽  
Bernardo Remuzzi Zandoná ◽  
Daniella de Moura Coelho ◽  
Ângela Malysz Sgaravatti ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Oxidative Damage ◽  
Antioxidant Defenses ◽  
Acute Administration ◽  
Young Rats

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

Aflatoxin B1 reduces non-enzymatic antioxidant defenses and increases protein kinase C activation in the cerebral cortex of young rats

2017 ◽  
Vol 21 (4) ◽  
pp. 268-275 ◽  
Author(s):  
Naiéli Schiefelbein Souto ◽  
Ana Claudia Monteiro Braga ◽  
Mayara Lutchemeyer de Freitas ◽  
Michele Rechia Fighera ◽  
Luiz Fernando Freire Royes ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Aflatoxin B1 ◽  
Antioxidant Defenses ◽  
Enzymatic Antioxidant ◽  
Young Rats ◽  
Kinase C ◽  
Protein Kinase C Activation

scholarly journals Sex Differences in Postischemic Neuronal Necrosis in Gerbils

1991 ◽  
Vol 11 (2) ◽  
pp. 292-298 ◽  
Author(s):  
Edward D. Hall ◽  
Kay E. Pazara ◽  
Kelley L. Linseman
Keyword(s):  
Lipid Peroxidation ◽  
Cerebral Cortex ◽  
Vitamin E ◽  
Protective Efficacy ◽  
Neuronal Population ◽  
Mongolian Gerbils ◽  
Neuronal Necrosis ◽  
Male And Female ◽  
Endogenous Estrogen

Twenty-four hour postischemic neuronal necrosis was compared in male vs. female Mongolian gerbils subjected to a 3-h period of severe incomplete hemispheric ischemia produced by unilateral carotid occlusion. The incidence of stroke-prone males was 42.9% versus 26.7% for the females. Among the stroke-prone animals, the males displayed significantly greater neuronal necrosis at 24 h after ischemia compared to the females in the cerebral cortex and CA, region of the hippocampus. In the CA, region of the stroke-prone males, only 2.0% of the normal neuronal population remained by 24 h compared to 36.8% in the stroke-prone females (p < 0.02). In the cerebral cortex, the males had only 19.9% of normal versus 58.2% in the females (p < 0.05). In a second series of mechanistic experiments, no differences in cortical blood flow (CBF) were disclosed between preselected male and female stroke-prone animals before, during, or for 2 h after ischemia. As with the CBF, the extent of cortical extracellular hypocalcia during ischemia did not differ significantly. However, the degree of postischemic recovery of cortical extracellular calcium was significantly better in the females from 30 min to 2 h after reperfusion. In the same experiments, hemispheric vitamin E levels were measured at the 2 h time point as an index of postischemic brain lipid peroxidation. No difference in baseline vitamin E levels was observed between male and female sham-operated gerbils. In the males subjected to 3 h of ischemia plus 2 h of reperfusion, the hemispheric vitamin E decreased by 43.5% compared to the sham-operated males. In contrast, the females displayed only a 4.2% decline (p < 0.05 versus males). Previous studies showing the protective efficacy of antioxidants in this model have suggested an important role of oxygen radical-induced lipid peroxidation. Thus, it is proposed that the lesser ischemic vulnerability of females may be based upon an antioxidant effect of endogenous estrogen. Indeed, estrogen was found to be a more potent inhibitor of iron-catalyzed lipid peroxidation in brain tissue than vitamin E.

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