Lactoperoxidase-catalyzed lipid peroxidation of microsomal and artificial membranes

Buege, John A.; Aust, Steven D.

doi:10.1016/0304-4165(76)90236-1

Cited by 110 publications

(40 citation statements)

References 32 publications

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“…Although neither peroxidase release nor H202 production by mammalian eggs has yet been described, the presence of a peroxidase in the uterine fluid of certain species (8) raises the possibility that H202 generated by the fertilized egg may limit the survival of adjacent spermatozoa through its interaction with the uterine peroxidase. Since mammalian sperm are rich in polyunsaturated, long chain fatty acids (26), peroxidase-catalyzed reactions may cause their oxidation to fatty acid hydroperoxides (27,28) that are spermicidal (26,(29)(30)(31). Thus sperm, because of their unusual fatty acid composition, may be particularly susceptible to attack by peroxidase supplied either by the egg or the uterus.…”

Section: Discussionmentioning

confidence: 99%

Hydrogen peroxide production, chemiluminescence, and the respiratory burst of fertilization: Interrelated events in early sea urchin development

Foerder

Klebanoff

Shapiro

1978

Proc. Natl. Acad. Sci. U.S.A.

108

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After fertilization of the sea urchin, Strongylocentrotus purpuratus, a crosslinked fertilization membrane is formed; the crosslinks (dityrosine residues) are synthesized in a reaction catalyzed by an ovoperoxidase that is released from the cortical granules during fertilization. The substrate for ovoperoxidase activity, hydrogen peroxide, is generated by the egg coincident with the "respiratory burst" that follows parthenogenetic activation by the divalent ionophore A23187 or fertilization. This burst of oxygen consumption may be almost quantitatively accounted for by hydrogen peroxide evolution, as measured by the peroxidase-catalyzed quenching of scopoletin fluorescence. Neither the burst of oxygen consumption nor hydrogen peroxide production occurs when the inhibitor of cortical granule discharge, procaine, is present at fertilization.Fertilization or parthenogenetic activation with A23187 also is associated with a burst of light emission. This chemiluminescence is inhibited in vivo by inhibitors of the ovoperoxidase, such as 3-amino-1,2,4-triazole, phenylhydrazine, sulfite, or azide. A crude ovoperoxidase preparation catalyzes hydrogen peroxide-dependent chemiluminescence that is similarly inhibited. Thus, the bursts of oxygen uptake, peroxide production, and chemiluminescence appear to be several manifestations of the peroxidative system released at fertilization. This system may additionally be responsible for spermicidal activity and thus may act as a component of the block to polyspermy. One of the early biochemical observations on the activation of egg metabolism at fertilization was that of Otto Warburg (1), who noted a marked increase in oxygen consumption on fertilization of sea urchin eggs. This observation has been confirmed with eggs of several different species (2). Oxygen consumption incb eases in an initial burst to reach a maximum at about 2 min post-fertilization and then falls to a plateau level slightly higher than that present before fertilization (3, 4). The metabolic basis for this respiratory burst is not known.In a study of fertilization-induced alterations in the egg of the sea urchin, Strongylocentrotus purpuratus, we found (5) that the glycoprotein coat on the egg surface is converted into a rigid, relatively impermeable "fertilization membrane" by the formation of crosslinks between tyrosine residues. The formation of the di-and trityrosine structures is catalyzed by an ovoperoxidase that is released from cortical granules in a massive exocytosis which occurs within seconds of fertilization (6). The occurrence of such a peroxidase-mediated reaction in the vicinity of the fertilized egg implies that the substrate for that enzyme, hydrogen peroxide (H202), is either formed or liberated by the egg with kinetics appropriate to its involvement in the crosslinking reaction. In this paper, we show that the egg does produce H202 at the appropriate time, and, additionally,The costs of publication of this article were defrayed in part by the payment of page charges. This article mu...

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Section: Discussionmentioning

confidence: 99%

Hydrogen peroxide production, chemiluminescence, and the respiratory burst of fertilization: Interrelated events in early sea urchin development

Foerder

Klebanoff

Shapiro

1978

Proc. Natl. Acad. Sci. U.S.A.

108

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“…A breakdown product of lipid peroxidation, thiobarbituric acidreactive substance (TBARS), was measured by the method of Buege and Aust (1976). Briefly, the stock solution contained equal volumes of 15% (w/v) trichloroacetic acid in 0.25 N hydrochloric acid and 0.37% (w/v) 2-thiobarbituric acid in 0.25 N hydrochloric acid.…”

Section: Lipid Peroxidationmentioning

confidence: 99%

Induction of oxidative stress in the rat testis after short-term exposure to the organochlorine pesticide methoxychlor

Latchoumycandane

Mathur

2002

Archives of Toxicology

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The ability of 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) to induce oxidative stress in various tissues of animals has been reported. The nature and mechanism of action of TCDD on the antioxidant system of sperm has not been studied. In the present study we have sought to investigate whether TCDD induces oxidative stress in the epididymal sperm of rats. Subchronic doses of TCDD (1, 10, and 100 ng/kg body weight per day) were administered orally to male Wistar strain rats for 45 days. After 24 h of the last treatment the rats were killed using diethyl ether. The epididymides were removed and cleared from the adhering tissues. Epididymal sperm were collected by cutting the epididymides into small pieces in Ham's F12 medium, and counted using a hemocytometer. The epididymal sperm counts in the TCDD-treated groups decreased in a dose-dependent manner from the control value of 8.2+/-0.14 x 10(8) to 5.31+/-0.15 x 10(8). Since a positive correlation (r=0.95; n=24) was observed between sperm count and DNA content of the epididymal sperm, DNA content was routinely used as an indicator of sperm count, and the results were expressed in terms of both protein and DNA. There was a significant decline in the activities of superoxide dismutase (40+/-2.17 to 27.1+/-0.76/mg protein and 32.41 to 18.07+/-0.76/mg DNA), catalase (2.49+/-0.13 to 2.03+/-0.05/mg protein and 2.01+/-0.05 to 1.35+/-0.05/mg DNA), glutathione reductase (71.2+/-3.87 to 48+/-1.79/mg protein and 57.58+/-1.52 to 31.94/mg DNA) and glutathione peroxidase (22.4+/-1.43 to 16.9+/-1.57/mg protein and 18.08+/-0.61 to 11.38+/-1.22/mg DNA) while there were increases in the levels of hydrogen peroxide (20.8+/-1.96 to 55.3+/-0.88/ mg protein and 16.18+/-1.88 to 36.87+/-0.88/ mg DNA) and lipid peroxidation (2.17+/-0.2 to 6.08/mg protein and 1.75+/-0.12 to 4.05+/-0.12/mg DNA) in the epididymal sperm. The results suggest that graded doses of TCDD elicit depletion of antioxidant defense system in sperm, indicating TCDD-induced oxidative stress in the epididymal sperm. In conclusion, the adverse effect on male reproduction in TCDD-treated rats may be due to the induction of oxidative stress in sperm.

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“…Plasma TBARS levels were measured according to the method of Buege and Aust [9] and Lapenna et al [10] . Briefly, 0.5 ml of ethylene diamine tetra-acetic acid plasma was added to a reaction mixture (1.0 ml) formed by equal parts of 15% trichloroacetic acid, 0.25 N hydrochloric acid, and 0.375% thiobarbituric acid, plus 2.5 m M butylated hydroxytoluene and 0.1 ml of 8.1% sodium dodecyl sulfate, followed by 30 min heating at 95 ° C; pH value of the analytical reaction mixture was about 0.9.…”

Section: Methodsmentioning

confidence: 99%

Plasma Thiobarbituric Acid-Reactive Substance Levels in Subclinical Hypothyroidism

Kebapçılar¹,

Akıncı²,

Bayraktar³

et al. 2007

Med Princ Pract

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Objective: The purpose of this study was to determine thiobarbituric acid-reactive substance (TBARS) levels in subclinical hypothyroidism and to examine the effect of levothyroxine replacement on TBARS levels. Subjects and Methods: A cohort of 28 female patients with subclinical hypothyroidism and 24 healthy controls were enrolled in this study. The levels of plasma TBARS, serum lipids, and high-sensitive C-reactive protein (CRP) in patients with subclinical hypothyroidism at baseline and after achieving euthyroid state by levothyroxine were assessed. Results: TBARS levels of the patients were similar to those of the control group in the subclinical hypothyroid state and after restoration of euthyroidism by levothyroxine replacement. TBARS levels decreased after levothyroxine treatment, but did not reach statistical significance. There was no significant correlation between TBARS, lipid and CRP levels. Serum CRP levels were higher in subclinical hypothyroidism (4.28 ± 0.9 mg/l) than in the control group (1.95 ± 0.34 mg/l) and the difference was statistically significant (p = 0.03). After achieving euthyroid state, CRP levels decreased significantly in patients with subclinical hypothyroidism from 4.28 ± 0.9 to 2.32 ± 0.6 mg/l (p = 0.006). Conclusion: Our findings suggest that there is no significant alteration of plasma TBARS levels neither in subclinical hypothyroid state nor after achieving euthyroid state. Serum CRP level is higher in patients with subclinical hypothyroidism than in the control group. Normalization of thyroid state seems to effectively reduce serum CRP levels in subclinical hypothyroidism without any correlation with TBARS activity.

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Lactoperoxidase-catalyzed lipid peroxidation of microsomal and artificial membranes

Cited by 110 publications

References 32 publications

Hydrogen peroxide production, chemiluminescence, and the respiratory burst of fertilization: Interrelated events in early sea urchin development

Hydrogen peroxide production, chemiluminescence, and the respiratory burst of fertilization: Interrelated events in early sea urchin development

Induction of oxidative stress in the rat testis after short-term exposure to the organochlorine pesticide methoxychlor

Plasma Thiobarbituric Acid-Reactive Substance Levels in Subclinical Hypothyroidism

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