Study of the protection of zinc and alpha-tocopherol on human sperm parameters, lipid peroxidation, apoptosis and DNA fragmentation with Mobile Phone Radiation treated in vitro

Previously we demonstrated that in vivo exposure of humans to NO2 resulted in significant inactivation of alpha 1-protease inhibitor (alpha 1-PI) in the bronchoalveolar lavage fluid. However, alpha 1-PI retains its elastase inhibitory activity in vitro when exposed to 10 times the concentration of NO2 used in vivo. We suggested exogenous oxidants such as O2 and NO2 exert their effect in vivo in part through lipid peroxidation. We investigated the mechanism of inactivation of alpha 1-PI in the presence or absence of lipids under oxidant atmosphere. alpha 1-PI in solutions containing phosphate buffer (control), 0.1 mM stearic acid (saturated fatty acid, 18:0), or 0.1 mM linoleic acid (polyunsaturated fatty acid, 18:2) was exposed to either N2 or NO2 (50 ppm for 4 h). Elastase inhibitory capacity of alpha 1-PI was significantly diminished in the presence of 0.1 mM linoleic acid and under NO2 atmosphere (75 +/- 8% of control, P less than 0.01), whereas there was no change in elastase inhibitory capacity of alpha 1-PI in the presence or absence (buffer only) of 0.1 mM stearic acid under a similar condition (109 +/- 11 and 94 +/- 6%, respectively). The inactivated alpha 1-PI as the result of peroxidized lipid could be reactivated by dithiothreitol and methionine sulfoxide peptide reductase, suggesting oxidation of methionine residue at the elastase inhibitory site. Furthermore the inhibitory effect of peroxidized lipid on alpha 1-PI could be prevented by glutathione and glutathione peroxidase and to some extent by alpha-tocopherol.

Download Full-text

Mécanisme moléculaire de l'effet protecteur de la vitamine E dans l'athérosclérose

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y02-076 ◽

2002 ◽

Vol 80 (7) ◽

pp. 662-669 ◽

Cited By ~ 4

Author(s):

Abdelouahed Khalil

Keyword(s):

Lipid Peroxidation ◽

Vitamin E ◽

Vascular Diseases ◽

Epidemiologic Studies ◽

Low Density Lipoproteins ◽

Alpha Tocopherol ◽

Low Density ◽

Prooxidant Effect

Oxidation of low-density lipoproteins constitutes the first step of a very complex process leading to atherosclerosis. Vitamin E, and principally alpha-tocopherol, is considered as the principal inhibitor of lipid peroxidation. Some studies showed the beneficial role of vitamin E in the prevention and reduction of atherosclerosis and its associated pathologies. However, other in vitro studies advance a prooxidant role of vitamin E. The results of the epidemiologic studies are difficult to generalize without taking account of the clinical randomized tests. In this work, we reviewed the principal studies devoted to the role of vitamin E and discussed the assumption of a prooxidant effect of this molecule.Key words: vitamin E, low-density lipoproteins (LDL), lipid peroxidation, cardio-vascular diseases.

Download Full-text

Cardioselective Ammonium, Phosphonium, and Sulfonium Analogs of .alpha.-Tocopherol and Ascorbic Acid That Inhibit in Vitro and ex Vivo Lipid Peroxidation and Scavenge Superoxide Radicals

Journal of Medicinal Chemistry ◽

10.1021/jm00015a010 ◽

1995 ◽

Vol 38 (15) ◽

pp. 2880-2886 ◽

Cited By ~ 20

Author(s):

J. Martin Grisar ◽

Gilbert Marciniak ◽

Frank N. Bolkenius ◽

Joelle Verne-Mismer ◽

Eugene R. Wagner

Keyword(s):

Lipid Peroxidation ◽

Ascorbic Acid ◽

Ex Vivo ◽

Superoxide Radicals ◽

Alpha Tocopherol

Download Full-text

Suppression of lipid peroxidation in adrenal microsomes following ACTH administration to guinea pigs

Journal of Endocrinology ◽

10.1677/joe.0.1680333 ◽

2001 ◽

Vol 168 (2) ◽

pp. 333-338 ◽

Cited By ~ 2

Author(s):

JM Burczynski ◽

JM Voigt ◽

PA Longhurst ◽

HD Colby ◽

Keyword(s):

Lipid Peroxidation ◽

Guinea Pigs ◽

Beta Carotene ◽

Alpha Tocopherol ◽

Inhibitory Effects ◽

Hormone Production ◽

Adrenal Hormone ◽

Acth Treatment ◽

Dose Dependent

Previous studies demonstrated high levels of lipid peroxidation (LP) in the guinea pig adrenal cortex. The present studies were done to determine if adrenal LP activity was influenced by ACTH, the major hormonal regulator of the gland. Guinea pigs were treated with ACTH for 1, 3 or 7 days. In addition, some guinea pigs received ACTH for 7 days and were killed 3 or 7 days later. After treatment, adrenal microsomal fractions were prepared and incubated in vitro with 1 mM ferrous sulfate to initiate LP. ACTH treatment caused a progressive decrease in adrenal LP; activity was almost totally inhibited within 3 days. The inhibitory effects of ACTH on LP were dose-dependent. Following cessation of ACTH treatment, adrenal LP gradually returned toward control levels. Microsomal concentrations of linoleic acid, a major substrate for adrenal LP, were increased by ACTH administration and then also returned to control levels after cessation of treatment. There were no significant changes in adrenal alpha-tocopherol or beta-carotene concentrations resulting from ACTH treatment. The results indicate that ACTH has a role in the regulation of adrenal LP. The actions of ACTH cannot be attributed to an increase in adrenal content of the antioxidants, alpha-tocopherol and beta-carotene, or to a decrease in LP substrate. The actions of ACTH to inhibit LP may contribute to an increase in adrenal hormone production by protecting steroidogenic enzymes from peroxidative degradation.

Download Full-text