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PubMed2000

Cadmium-induced liver, heart, and spleen lipid peroxidation in rats and protection by selenium.

The purpose of this study was to evaluate the effects of cadmium-induced peroxidative damage to rat liver, heart, and spleen. Sprague-Dawley rats were injected subcutaneously with a single dose of 25, 125, 500, or 1250 microg Cd/kg and evaluated 6, 12, 24, or 72 h later. Liver, heart, and spleen were analyzed for lipid peroxidation and Fe, Cu, Zn, Se, and Cd concentrations. Data showed that Cd produced enhanced lipid peroxidation in the liver, heart, and spleen. These Cd-induced changes were accompanied by a significant rise in liver, heart, and spleen Fe and Cu, and a fall in spleen Zn and liver, heart, and spleen Se. Concurrent treatment with Se and Cd reduced the Cd-induced alterations in liver, heart, and spleen peroxidation and essential metal levels. Data suggest that lipid peroxidation is associated with cadmium toxicity and that Se was found effective in preventing lipid peroxidation.

Animals↗
PubMed2004

Oxidative stress: potential of distinct peroxide determination systems.

When reactive oxygen species attack biological structures, peroxides, which are short-lived oxidative intermediates, are generated. We evaluated the potential of two different, commercially available peroxide activity assays (Pox-Act and d-ROMS) to see whether the results were associated with the clinical condition of subjects who were participating in a routine health care program. Furthermore, we determined the total antioxidant status (TAS) and the titer of autoantibodies against oxidized low-density lipoprotein (oLAb) to verify the hydroperoxide measurements. Subjects with medical conditions (hereafter referred to as patients) had significantly increased serum peroxide levels compared to healthy subjects. The d-ROMS kit indicated that 86% of subjects had an increased level of total peroxides. Although the assays had a significant correlation (p<0.001), 34% of the subjects had an increased total peroxide concentration in the Pox-Act assay that was clearly associated with clinical symptoms. Furthermore, the sensitivity of the Pox-Act assay was 35 times higher than that of the d-ROMS kit. In subjects with medical conditions, there was a trend toward a decreased TAS and a slightly increased oLAb titer in comparison to healthy subjects, but this was not statistically significant. The Pox-Act assay seems to be a valuable tool for the determination of total peroxides, while the results from the d-ROMS kit should be considered with caution.

Adult↗
PubMed1995

The in vitro effects of captopril on the levels of lipid peroxidation and glutathione of erythrocytes in type II diabetes.

Increase in lipid peroxidation (LP) is an indirect marker of free radical activation. The products of LP (malonyldialdehyde: MDA) are increased in diabetic patients, particularly those with angiopathy. Free radicals are eliminated by cellular enzymes such as superoxide dismutase, catalase and glutathione peroxidase. In this study, the effect and the mechanism of action of captopril, and angiotensin converting enzyme (ACE) inhibitor, on lipid peroxidation in erythrocytes from diabetics was investigated. LP and glutathione were studied in 10 type II diabetics (mean age: 57 +/- 10 yr, duration of diabetes: 12 +/- 6 yr) and in 10 healthy subjects (mean age: 30 +/- 5 yr). Lipid peroxidation levels were 20.69 +/- 4.68 MDA% in diabetics and 9.62 +/- 1.87 MDA% in normal subjects. The LP in erythrocytes of type II diabetics was decreased by the increasing concentrations of captopril (before captopril: 20.69 +/- 4.68, after captopril: (2 x 10(-5) M) 16.68 +/- 7.49 MDA%; (4 x 10(-5) M) 14.17 +/- 7.65 MDA%; (6 x 10(-5) M) 12.33 +/- 2.8 MDA%). No difference was found in the inhibition of LP between the captopril concentrations of 6 x 10(-5) M and 10 x 10(-5) M. After preincubation with captopril, the glutathione level did not change significantly in the diabetic and normal erythrocytes. Preincubation with 2-6 x 10(-5) M captopril showed no effect in the normal group (p > 0.05) but 10 x 10(-5) M captopril reduced lipid peroxidation (p < 0.01). In our study, the high levels of lipid peroxidation in erythrocytes from diabetic patients were decreased after preincubation with captopril. Decrease in the level of lipid peroxidation in vitro was independent of the glutathione level. Crosslink binding between MDA and captopril is suggested.

Adult↗
PubMed1992

Cerebral lipid peroxidation in the growth retarded rat fetus under normoxia and hypoxia.

To detect a possible relationship between the increased vulnerability of the brain of the growth retarded fetus and lipid peroxidation, the activity of the latter was investigated in the forebrain of rat fetuses on day 22 of gestation (term = 23). Growth retardation was induced by uterine artery ligation on day 18. The susceptibility of the forebrain to lipid peroxidation was analysed using the thiobarbituric acid technique after exposure of the awake dams to room air or hypoxia (10% O2) for 58 minutes. Hemodynamics and blood gas status in the dams were stable under conditions of normoxia. When exposed to hypoxia, oxygen availability decreased and blood pressure fell slightly. When normalised for litter, lipid peroxidation covaried with fetal weight in fetuses from normoxic dams, only when Fe2+ (a promotor of lipid peroxidation) was added in the incubation. In fetuses from hypoxic dams, this relationship existed irrespective of whether Fe2+ was present during incubation. In all of these associations, smaller fetuses exhibited more intense lipid peroxidation. In the perinatal period, an increased vulnerability of the central nervous system prevails in growth retarded individuals. An increased tendency to undergo lipid peroxidation and/or a weak defence against this process may be part of the pathophysiologic background.

Animals↗
PubMed2001

Regulation of lipid peroxidation by nitric oxide and PGF2alpha during luteal regression in rats.

Corpus luteum regression is related to an increased generation of reactive oxygen species. Although several studies indicate that PGF(2alpha) is involved in regression of the corpus luteum in mammalian species through an increase in reactive oxygen species, the exact mechanism remains unknown. In the present study, the relationship between nitric oxide and PGF(2alpha) in regulation of lipid peroxidation was studied. Ovarian tissue from pseudopregnant rats at mid- (day 5) or late phase or at the time of regression (day 9 of pseudopregnancy) of corpus luteum development was used. Thiobarbituric acid reactants, used as a lipid peroxidation index, were higher on day 9 of pseudopregnancy than on day 5. In contrast, glutathione content (an antioxidant metabolite) was lower on day 9 than on day 5 of pseudopregnancy. These results indicate that there was an enhanced oxidative status in ovarian tissue during luteolysis. Administration of N(omega)-nitro-L-arginine methyl ester (L-NAME: 600 micromol l(-1)), a competitive nitric oxide synthase (NOS) inhibitor, led to a decrease in basal thiobarbituric acid reactant content in ovarian tissue from rats on day 9 of pseudopregnancy only, indicating that during regression of the corpus luteum, NO could act as intermediary in ovarian lipid peroxidation. Administration of a luteolytic dose (3 microg kg(-1) body weight i.p.) of a synthetic PGF(2alpha) increased thiobarbituric acid reactant content in ovaries from rats on day 9 of pseudopregnancy. As this effect was reversed partially by L-NAME, it is proposed that during regression of corpora lutea, PGF(2alpha) and NO are involved in regulation of lipid peroxidation. As this effect was only reversed partially, it is possible that there is another mechanism involving PGF(2alpha) (but not the NO-NOS pathway) in regulation of ovarian lipid peroxidation. Furthermore, the administration of PGF(2alpha) enhanced ovarian NOS activity, whereas cyclooxygenase inhibition (by indomethacin treatment in vivo) reduced it. As western blotting of ovarian homogenates obtained from PGF(2alpha)-injected rats increased inducible NOS (iNOS) content, it is concluded that PGF(2alpha) enhances both activity and synthesis of NO in rat ovarian tissues during luteolysis. Taken together, these results indicate that in ovaries with regressing corpora lutea, both NO and PGF(2alpha) are involved in part in regulation of lipid peroxidation.

Animals↗
PubMed2004

Elevated levels of erythrocyte-conjugated dienes indicate increased lipid peroxidation in schistosomiasis mansoni patients.

Schistosoma mansoni causes liver disease by inducing granulomatous inflammation. This favors formation of reactive oxygen species, including superoxide ions, hydrogen peroxide and hydroxyl radicals all of which may induce lipid peroxidation. We have evaluated lipid peroxidation in 18 patients with hepatosplenic schistosomiasis mansoni previously treated with oxamniquine followed by splenectomy, ligature of the left gastric vein and auto-implantation of spleen tissue, by measuring levels of erythrocyte-conjugated dienes and plasma malondialdehyde (MDA). Age-matched, healthy individuals (N = 18) formed the control group. Erythrocyte-conjugated dienes were extracted with dichloromethane/methanol and quantified by UV spectrophotometry, while plasma MDA was measured by reaction with thiobarbituric acid. Patient erythrocytes contained two times more conjugated dienes than control cells (584.5 +/- 67.8 vs 271.7 +/- 20.1 micromol/l, P < 0.001), whereas the increase in plasma MDA concentration (about 10%) was not statistically significant. These elevated conjugated dienes in patients infected by S. mansoni suggest increased lipid peroxidation in cell membranes, although this was not evident when a common marker of oxidative stress, plasma MDA, was measured. Nevertheless, these two markers of lipid peroxidation, circulating MDA and erythrocyte-conjugated dienes, correlated significantly in both patient (r = 0.62; P < 0.01) and control (r = 0.57; P < 0.05) groups. Our data show that patients with schistosomiasis have abnormal lipid peroxidation, with elevated erythrocyte-conjugated dienes implying dysfunctional cell membranes, and also imply that this may be attenuated by the redox capacity of antioxidant agents, which prevent accumulation of plasma MDA.

Adolescent↗
PubMed1996

Cultured rat mesothelial cells generate hydrogen peroxide: a new player in peritoneal defense?

This study was designed to examine whether rat peritoneal mesothelial cells in culture could generate hydrogen peroxide in different experimental conditions. Mesothelial cells, incubated in M-199, spontaneously released hydrogen peroxide. This process was significantly increased by addition of phorbol myristate acetate, as well as of superoxide dismutase to the medium, whereas it was substantially inhibited by catalase. Exposure of mesothelial cells to modified M-199 medium with 1.5% glucose concentration-lactated peritoneal dialysis solution did not seem to interfere either with the spontaneous release of hydrogen peroxide, or with that induced by phorbol myristate acetate. Furthermore, exposure of mesothelial cells to the glucose (4.25%) peritoneal dialysis solution in Medium M-199, was coincident with increased hydrogen peroxide generation, which was significantly higher than the spontaneous release, and not far from that observed with phorbol myristate acetate and superoxide dismutase. So far, it can be inferred from this evidence that peritoneal mesothelial cells in culture are not only endowed with the capability of producing hydrogen peroxide, but they can also be activated to do so in a way comparable to that observed in neutrophils and macrophages. This attribute is one more indication that mesothelial cells play a relevant role in the peritoneal mechanism of defense against infection. On the other hand, continuous exposure of mesothelial cells to glucose-enriched fluids, as occurs in clinical continuous ambulatory peritoneal dialysis, may well also be at the origin of a process of continuous injury, resulting from an increased hydrogen peroxide generation.

Animals↗
PubMed1986

Effects of hydrogen peroxide on oral carcinogenesis in hamsters.

The effects of twice weekly topical applications of hydrogen peroxide on the buccal epithelium of Syrian hamsters were studied. Animals were treated either with hydrogen peroxide alone, with hydrogen peroxide and the carcinogen 9, 10-dimethyl-1,2-benzanthracene (DMBA), or with DMBA alone. In animals treated with 30% H2O2 alone, histopathologic examination after 22 weeks revealed hyperkeratosis and hyperplasia in all animals with hyperchromatic cells and mild dysplasia in four of nine: no tumors were seen. In animals treated with DMBA alone, three of seven (43%) developed epidermoid carcinoma, while six of 11 (55%) of animals treated with DMBA plus 3% hydrogen peroxide and five of five (100%) of animals treated with DMBA plus 30% hydrogen peroxide (P = 0.054) developed carcinoma. Thus, hydrogen peroxide can, by itself, induce pathologic changes frequently associated with preneoplastic lesions; it may also augment carcinogenesis associated with DMBA.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1995

Hydrogen peroxide: a review of its use in dentistry.

Several dentifrices that contain hydrogen peroxide are currently being marketed. The increased use of bleaching agents containing (or generating) H2O2 prompted this review of the safety of H2O2 when used in oral hygiene. Daily exposure to the low levels of H2O2 present in dentifrices is much lower than that of bleaching agents that contain or produce high levels of H2O2 for an extended period of time. Hydrogen peroxide has been used in dentistry alone or in combination with salts for over 70 years. Studies in which 3% H2O2 or less were used daily for up to 6 years showed occasional transitory irritant effects only in a small number of subjects with preexisting ulceration, or when high levels of salt solutions were concurrently administered. In contrast, bleaching agents that employ or generate high levels of H2O2 or organic peroxides can produce localized oral toxicity following sustained exposure if mishandled. Potential health concerns related to prolonged hydrogen peroxide use have been raised, based on animal studies. From a single study using the hamster cheek pouch model, 30% H2O2 was referred to as a cocarcinogen in the oral mucosa. This (and later) studies have shown that at 3% or less, no cocarcinogenic activity or adverse effects were observed in the hamster cheek pouch following lengthy exposure to H2O2. In patients, prolonged use of hydrogen peroxide decreased plaque and gingivitis indices. However, therapeutic delivery of H2O2 to prevent periodontal disease required mechanical access to subgingival pockets. Furthermore, wound healing following gingival surgery was enhanced due to the antimicrobial effects of topically administered hydrogen peroxide. For most subjects, beneficial effects were seen with H2O2 levels above 1%.

Animals↗
PubMed1990

Dynamic microstructure and hydration of peroxidized membrane of rat cardiac mitochondria and effects of adriamycin.

Nanosecond time-resolved fluorometry of diphenyl hexatriene, DPH, fluorescence was used to study the effects of lipid peroxidation caused by NADH or adriamycin treatment on the dynamic microstructure of mitochondrial membranes from rat myocardium. Isolated mitochondria were incubated with NADH, FeCl3, and ADP, or with adriamycin. Parameters for microdynamics were calculated from the fluorescence intensity and anisotropy decay curves for DPH fluorescence. Peroxidized lipids were measured as malondialdehyde (MDA) resulting from the thiobarbiturate reaction. As peroxidized lipids accumulated, the membrane viscosity increased and the wobbling angle of the phospholipids decreased. The structural changes induced in unsaturated phospholipids by peroxidation probably increased the friction of neighboring phospholipids and restricted the range of their wobbling motion. The fluorescence intensity and fluorescence lifetimes decreased significantly when MDA was higher than 10 nmol/mg protein. These alterations in the behavior of DPH fluorescence strongly suggest that the hydration of the phospholipid layer of the mitochondria is occurring as a consequence of lipid peroxidation, since the fluorophore, DPH, is hydrophobic and its fluorescence is known to be quenched by increasing the dielectric constant of the surrounding media. The present results provide experimental supports to the hypothesis of membrane hydration induced by lipid peroxidation.

Animals↗
PubMed2001

Effects of chlorhexidine digluconate and hydrogen peroxide on Porphyromonas gingivalis hemin binding and coaggregation with oral streptococci.

Porphyromonas gingivalis, a gram-negative anaerobe, is one of the major causative agents of periodontal disease. In this study, the effects of chlorhexidine digluconate and hydrogen peroxide on the hemin binding of P. gingivalis and coaggregation of this bacterium with oral streptococci were examined. The pretreatment of P. gingivalis W50 and 381 with chlorhexidine digluconate and hydrogen peroxide increased the hemin binding of these bacteria. The hemin binding of P. gingivalis was increased by the subminimal inhibitory concentration (MIC) of chlorhexidine digluconate. However, concentrations of hydrogen peroxide below the MIC had no effect on the hemin binding of P. gingivalis W50 and 381. Coaggregation of P. gingivalis 381 with Streptococcus oralis ATCC 9811 and Streptococcus gordonii DL1 was diminished by chlorhexidine digluconate. The coaggregation-inhibitory effect was concentration-dependent. Hydrogen peroxide also showed inhibitory effects on the coaggregation of P. gingivalis 381 with S. oralis 9811 and S. gordonii DL1 at concentrations below that used clinically. Concentrations of chlorhexidine digluconate below the MIC inhibited coaggregation. However, concentrations of hydrogen peroxide below the MIC were not effective in reducing the coaggregation of P. gingivalis with oral streptococci. These observations show that chlorhexidine digluconate and hydrogen peroxide could confer variable effects on P. gingivalis hemin binding and coaggregation of this bacterium with oral streptococci.

Anti-Infective Agents, Local↗
PubMed1989

Erythrocyte membrane lipid peroxidation and glycosylated hemoglobin in diabetes.

Erythrocytes of diabetic patients have abnormal membrane properties. We examined in vivo membrane lipid peroxidation in erythrocytes of diabetic subjects and its possible relationship with hyperglycemia. Lipid peroxidation was assessed in fresh, untreated erythrocytes by quantitating thiobarbituric acid reactivity and an adduct of phospholipids and malonyldialdehyde (MDA), an end product of lipid peroxidation, with thin-layer chromatography of lipid extract of diabetic erythrocytes. There was a significantly increased membrane lipid peroxidation in diabetic erythrocytes compared with nondiabetic erythrocytes. The degree of membrane lipid peroxidative damage in erythrocytes was significantly correlated with the level of glycosylated hemoglobin, an index of mean glucose level for the preceding 3-4 mo. This suggests that peroxidation of membrane lipids and accumulation of MDA occurs in erythrocytes of diabetic patients.

Diabetes Mellitus↗
PubMed1990

Modulation of lipid peroxidation in human spermatozoa and human prostate by prostatic inhibin.

Loss of sperm motility as a result of the production of hydrogen peroxide by lipid peroxidation is regulated by as yet unidentified prostatic factor(s). Inhibinlike peptide of prostatic origin isolated from human seminal plasma, with a molecular size of about 10,400 daltons, was studied for its effect on ascorbate-induced lipid peroxidation in human spermatozoa. Dose-related suppression of lipid peroxidation was observed at dose levels of 0.25, 0.5, and 1.0 micrograms. The data suggest that inhibinlike peptide could be one of the factors involved in the regulation of lipid peroxidation and thereby of sperm motility. Inhibinlike peptide also exhibited local action in both normal and benign hyperplastic human prostate tissue by enhancing the rate of lipid peroxidation. These findings have implications in the pathophysiology of the prostate.

Dose-Response Relationship, Drug↗
PubMedDate not supplied

Magnolol protects human sperm motility against lipid peroxidation: a sperm head fixation method.

It was previously reported that magnolol, isolated from the Chinese medicinal herb Magnolia officinalis, had a potent inhibitory activity on lipid peroxidation. Since sperm motility could be suppressed by lipid peroxidation, this study examines the protective effect of magnolol on lipid peroxidation-suppressed sperm motility. FeSO4 was used to induced lipid peroxidation and sperm motility was expressed as tail beat frequency (TBF) measured with a sperm head fixation method. Magnolol at 10(-9) to 10(-7) M significantly reversed the FeSO4-suppressed TBF. Magnolol significantly inhibited the generation of malondialdehyde (MDA), the end product of lipid peroxidation, in sperm. Magnolol protected sperm motility by inhibiting lipid peroxidation in sperm.

Biphenyl Compounds↗
PubMed1996

Lipid peroxidation: a review of causes, consequences, measurement and dietary influences.

In this review the process of lipid peroxidation and the atherogenicity of peroxidied lipids are discussed. Recent findings with regard to the effect of selected dietary factors on susceptibility of lipids to oxidative stress and on antioxidant defences are analysed with particular reference to their potential use in the prevention and treatment of atherogenesis and, by extension, coronary heart disease. Laboratory methods of assessing antioxidant defences, lipid peroxidation and the effects of lipid peroxidation are also reviewed and discussed with particular reference to their ability to assess in vivo oxidative stress and lipid peroxidation status. A range of oxidative stress indices are presented and their limitations discussed, but the main focus is on the most commonly used laboratory test for lipid peroxidation, the thiobarbituric acid reacting substances (TBARS) test. Finally, the influence of selected dietary factors on measured peroxidation status is discussed, with particular reference to the antioxidant vitamins C (ascorbic acid) and E (alpha tocopherol) and the type of fatty acids (mono- and poly-unsaturated) in the diet.

Antioxidants↗
PubMed1999

Serum and placental lipid peroxides in chronic hypertension during pregnancy with and without superimposed preeclampsia.

OBJECTIVE: To evaluate the circulating levels of lipid peroxides and vitamin E, and the placental levels of lipid peroxides in chronic hypertensive pregnant women, with and without superimposed preeclampsia, as compared to controls and women with primary preeclampsia. METHODS: Lipid peroxides were measured in serum and placenta by the thiobarbituric acid method and high-pressure liquid chromatography (HPLC), and vitamin E by HPLC. Patients were 36 healthy pregnant women, 34 previously nonhypertensive women diagnosed with preeclampsia, 20 women with uncomplicated chronic hypertension, and 11 women with chronic hypertension complicated by superimposed preeclampsia. RESULTS: Lipid peroxides in serum and placental tissue were significantly increased, and vitamin E levels in serum were significantly decreased in women with primary preeclampsia and superimposed preeclampsia, as compared to controls. The group of uncomplicated chronic hypertension presented with similar values of lipid peroxides and vitamin E to controls. CONCLUSIONS: Our results support the clinical assumption that chronic hypertension aggravated by the development of proteinuria represents a superimposed condition associated with placental disease. The data further support the concept that increased lipid peroxides are not merely associated with the presence of hypertension in pregnancy, but they are implicated in the pathophysiology of preeclampsia.

Case-Control Studies↗
PubMed1986

Comparison of the inactivation of microsomal glucose-6-phosphatase by in situ lipid peroxidation-derived 4-hydroxynonenal and exogenous 4-hydroxynonenal.

1) The effect of 4-hydroxynonenal and lipid peroxidation on the activities of glucose-6-phosphatase and palmitoyl CoA hydrolase were studied. 2) 4-Hydroxynonenal inactivates glucose-6-phosphatase but has no effect on palmitoyl-CoA hydrolase. These effects are similar with those observed during lipid peroxidation of microsomes. 3) The inhibition of glucose-6-phosphatase by 4-hydroxynonenal can be prevented by glutathione but not by vitamin E. The inactivation of glucose-6-phosphatase during lipid peroxidation is prevented by glutathione and delayed by vitamin E. 4) The formation of 4-hydroxynonenal during lipid peroxidation was followed in relation to the inactivation of glucose-6-phosphatase. At 50% inactivation of glucose-6-phosphatase the 4-hydroxynonenal concentration was 1.5 microM. To obtain 50% inactivation of glucose-6-phosphatase by added 4-hydroxynonenal a concentration of 150 microM or 300 microM was needed with a preincubation time of 30 and 60 min, respectively. 5) It is concluded that the glucose-6-phosphatase inactivation during lipid peroxidation can be due to the formation of 4-hydroxynonenal. The formed 4-hydroxynonenal which inactivates glucose-6-phosphatase is located in the membrane. If this mechanism is valid it implies that a functional SH group of glucose-6-phosphatase is layered in the membrane. However, an inactivation of glucose-6-phosphatase by desintegration of the membrane by lipid peroxidation cannot be ruled out.

Aldehydes↗
PubMed1987

Lipid peroxidation in choline-methionine deficiency.

A deficiency of choline and methionine is hepatocarcinogenic and is associated with an apparent increase in lipid peroxidation. In this study the susceptibility of microsomes and nuclei to ferritin-dependent lipid peroxidation is examined together with the status of the peroxidation-protective systems. Choline-methionine deficiency caused an increase in Se-independent GSH peroxidases (GSH transferase subunit 2) and membrane vitamin E but a decrease in Se-dependent GSH peroxidase and microsomal GSH peroxidase activity. Choline-methionine deficient microsomes and nuclei were 4-fold more susceptible to lipid peroxidation induced in vitro by physiological concentrations of ferritin/ascorbate/ADP; and the peroxidation was less effectively inhibited by GSH and soluble GSH peroxidases than controls. The results indicate that a decreased level of Se-dependent and membrane GSH peroxidases is involved in the increase in lipid peroxidation observed in choline-methionine deficiency.

Choline Deficiency↗