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PubMed1992

Lipid peroxidation in early experimental diabetes in rats: effects of diabetes and insulin.

The degree of lipid peroxidation was measured in organs from diabetic rats receiving no treatment, and in those from insulin-treated diabetic rats and controls. Lipid peroxidation was measured as organ content of malondialdehyde, a degradation product of polyunsaturated fatty acids. In the kidney, lipid peroxidation was increased after one week of diabetes; insulin treatment reduced the level of lipid peroxidation to levels lower than seen in controls. In the liver, diabetes caused an increased lipid peroxidation, which could be reversed by insulin; no additional effect of insulin was found. In heart and pancreas no effects of diabetes or insulin were demonstrated. The present paper provides evidence that lipid peroxidation is increased in the early stages of experimental diabetes and is reversible by insulin treatment. Hyperinsulinaemia may, in itself, counteract lipid peroxidation in kidney.

Animals↗
PubMed1977

Damage to ram spermatozoa by peroxidation of endogenous phospholipids.

We examined the damaging effects on spermatozoa of endogenous phospholipid peroxidation brought about by aerobic incubation at 37 degrees C in the presence of 0-5 mM-ascorbic acid and 0-5 mM-FeSO4. As well as becoming immotile, such peroxidized spermatozoa also lost, through leakage, certain intracellular enzymes into the surrounding medium, on a scale resembling that produced by cold shocking non-peroxidized spermatozoa. Morphological observations revealed that peroxidation damaged the plasma membrane, particularly in the region of the acrosome. Further experiments showed that lipid peroxidation irreversibly abolished the fructolytic and respiratory activity of spermatozoa. The susceptibility of spermatozoa to peroxidation was greater when the cells were damaged before incubation with ascorbic acid and FeSO4. To some extent, peroxidation could be prevented, but not reversed, by the addition to sperm suspensions of dialysed egg yolk or dialysed bull seminal plasma. However, dialysed seminal plasma from ram, stallion or man had no protective effect.

Animals↗
PubMed1984

The possible role of squalene and its peroxide of the sebum in the occurrence of sunburn and protection from the damage caused by U.V. irradiation.

To clarify the role of squalene peroxide in the occurrence of skin damage from sunburn, the optimum condition of squalene peroxidation and the effect of squalene peroxide on cutaneous tissue were examined. Peroxidation of squalene was more easily induced than palmitoleic acid and oleic acid in the unsaturated lipid occurred in sebum. The peroxidation of squalene gradually occurred by U.V. irradation, and it is parallel to increases in the malonyldialdehyde production (production of lipoperoxide). This peroxidation easily carries out in the case of high temperature (40 degrees C than 30 degrees C), and in the case of low pH. Good correspondence was recognized among the spectrum of natural daylight, U.V. absorption spectrum of squalene and erythema curve. Squalene and its peroxide have an important role in the occurrence of sunburn, and/or protection from damage caused by U.V. irradiation.

Animals↗
PubMed2006

Comparison of hydrogen peroxide and peracetic acid as isolator sterilization agents in a hospital pharmacy.

PURPOSE: The efficacy of hydrogen peroxide and peracetic acid as isolator sterilization agents was compared. METHODS: Sterilization and efficacy tests were conducted in a flexible 0.8-m3 transfer isolator using a standard load of glass bottles and sterile medical devices in their packing paper. Bacillus stearothermophilus spores were placed in six critical locations of the isolator and incubated at 55 degrees C in a culture medium for 14 days. Sterilization by 4.25 mL/m3 of 33% vapor-phase hydrogen peroxide and 12.5 mL/m3 of 3.5% peracetic acid was tested in triplicate. Sterility was validated for hydrogen peroxide and peracetic acid at 60, 90, 120, and 180 minutes and at 90, 120, 150, 180, 210, and 240 minutes, respectively. RESULTS: In an efficacy test conducted with an empty isolator, the sterilization time required to destroy B. stearothermophilus spores was 90 minutes for both sterilants, indicating that they have comparable bactericidal properties. During the validation test with a standard load, the sterilization time using hydrogen peroxide was 150 minutes versus 120 minutes with peracetic acid. The glove cuff was particularly difficult for hydrogen peroxide to sterilize, likely due to its slower diffusion time than that of peracetic acid. Hydrogen peroxide is an environmentally safer agent than peracetic acid; however, its bacteriostatic properties, lack of odor, and poor diffusion time may limit its use in sterilizing some materials. CONCLUSION: Hydrogen peroxide is a useful alternative to peracetic acid for isolator sterilization in a hospital pharmacy or parenteral nutrition preparation unit.

Disinfectants↗
PubMedDate not supplied

Hydrogen peroxide inhibits lung neutral endopeptidase.

Oxidants have been implicated in the pathogenesis of many inflammatory airway diseases. Neutral endopeptidase (also called enkephalinase, EC 3.4.24.11) is a peptidase that is involved in the degradation of several proinflammatory peptides, such as tachykinins and kinins. Indirect evidence suggests that airway neutral endopeptidase is inactivated by oxidants. To determine whether hydrogen peroxide inactivates neutral endopeptidase, we studied the activity of this peptidase in washed crude preparations of membranes from guinea pig lungs. Washed crude membrane preparations were exposed to increasing concentrations of hydrogen peroxide (1.25-25 mM) in the presence or absence of two different concentrations of catalase (300 and 700 U/mL). Neutral endopeptidase activity was inhibited by hydrogen peroxide in a concentration-dependent fashion (p = .0001). Addition of catalase prevented, in a concentration-dependent fashion, the inhibition of neutral endopeptidase induced by hydrogen peroxide (p = .0001). Mannitol (40 mM) and L-methionine (20 mM) did not prevent inhibition of neutral endopeptidase induced by hydrogen peroxide (2.5 mM). It can be concluded that neutral endopeptidase is inactivated by hydrogen peroxide, an effect that is prevented by catalase. Hydrogen peroxide-induced inactivation of neutral endopeptidase is not mediated by spontaneous generation of either hydroxyl radical or hypochlorous acid in the membrane preparation. Our results suggest that neutral endopeptidase inactivation may occur in airway diseases associated with exposure to or production of oxidants.

Animals↗
PubMed1985

Effect of lipid peroxidation on rhodopsin regeneration.

We have developed an in vitro system in which lipid peroxidation can be produced in a predictable fashion and have studied the effects of peroxidation on regenerability of rhodopsin in rod outer segments (ROS). ROS isolated by sucrose flotation from dark-adapted retinas of Rana pipiens were suspended in various concentrations of FeSO4 and 1 or 2 mM ascorbic acid for 10 minutes. An increase in lipid hydroperoxides (measured as conjugated dienes) and a decrease in 22:6 omega 3 were determined for each Fe+2 concentration and used as an index of peroxidation. Following incubation with and without FeSO4, ROS were pelleted and rhodopsin was regenerated with 15 micron 11-cis-retinal. The regenerability of rhodopsin in ROS in which significant lipid peroxidation had taken place was reduced by 40-50% compared to controls. DTPA (diethylenetriamine pentaacetic acid), EDTA, and EGTA protected against lipid peroxidation by Fe+2 and allowed almost complete regeneration of rhodopsin. Incubation with DTPA also prevented the destruction of vitamin E in ROS. Other compounds containing primary amine groups did not protect against peroxidation or loss of regenerability. These experiments indicate that lipid peroxidation is associated with a loss of regenerability of the visual pigment rhodopsin.

Animals↗
PubMed2001

The role of p38 MAP kinase in hydrogen peroxide mediated endothelial solute permeability.

OBJECTIVE: The purpose of this study was to determine the contribution of p38 MAP kinase activity during hydrogen peroxide mediated increased endothelial solute permeability. We also sought to identify the role of p38 MAP kinase-mediated changes in endothelial cell architecture due to hydrogen peroxide challenge. METHODS: Hydrogen peroxide mediated permeability of HUVEC was determined with and without inhibition of p38 MAP kinase by SB202190. Hydrogen peroxide mediated rearrangement of the endothelial actin cytoskeleton and junctional proteins occludin and ZO-1 were observed by immunofluorescence microscopy. RESULTS: Hydrogen peroxide treatment of endothelial monolayers caused a significant increase in solute permeability over a ninety-minute time period. Oxidant-mediated permeability and phosphorylation of p38 MAP kinase was significantly attenuated by SB 202190. Immunofluorescent staining for the tight junctional proteins occludin and ZO-1 demonstrated that oxidant challenge caused a loss of endothelial tight junction organization. Rhodamine phalloidin staining of the actin cytoskeleton showed that hydrogen peroxide stimulated increased stress fiber formation with concomitant gap formation between adjacent endothelial cells. Inhibition of p38 MAP kinase during oxidant challenge significantly attenuated actin stress fiber formation and prevented gap formation. CONCLUSIONS: These data demonstrate that p38 MAP kinase activity is involved in hydrogen peroxide mediated permeability, stress fiber formation, and intracellular gap formation.

Actin Cytoskeleton↗
PubMed1996

High potassium diets reduce vascular and plasma lipid peroxides in stroke-prone spontaneously hypertensive rats.

We examined the effect of high potassium (K) diet on oxidative stress to endothelium in hypertensive rats. Five-week-old stroke-prone spontaneously hypertensive rats (SHRsp) were fed a 5% high NaCl diet containing either 0.5% normal K (n = 28) or 2.1% high K (n = 19) for 6 weeks, and lipid peroxides in the aortic intima and plasma were measured. Lipid peroxides were extracted into an organic solvent to avoid the interference of carbohydrates or glycoproteins, and malondialdehyde (MDA) produced from lipid peroxides by acid-heating was measured by its reaction to thiobarbituric acid. The antioxidant butylated hydroxytoluene prevented spurious lipid peroxide formation during the whole procedure, and optimum Fe3+ allowed a maximum MDA production from lipid peroxides. The high K SHRsp showed lower lipid peroxide levels than the normal K SHRsp both in the intima (5.6 +/- 0.3 vs. 7.2 +/- 0.4 nmol MDA/mg fatty acids, p < 0.003) and plasma (0.91 +/- 0.08 vs. 1.46 +/- 0.10 nmol MDA/ml, p < 0.001). Mean arterial pressure was slightly lower by 13 mmHg in the high K SHRsp, but these differences were still obvious even when we compared groups of rats with precisely matching blood pressures. These results indicate that high K diets reduce oxidative stress on the endothelium of high NaCl-fed SHRsp independently of blood pressure changes. This effect may be involved in the mechanism by which high K diets protect endothelium and reduce stroke incidence in hypertensive animals. Thus, we improved the method of lipid peroxide measurement and propose the protective effects of high K diet against oxidative stress to endothelium in hypertension animals.

Animals↗
PubMed1983

Effect of the degradation of cytochrome P-450 heme by secobarbital on polychlorinated biphenyls (PCB)-induced hepatic vitamin A reduction and lipid peroxide formation in rats.

The present studies were conducted to characterize the relevance of a microsomal mixed function oxidase system to the polychlorinated biphenyls (PCB)-induced vitamin A reduction and endogenous lipid peroxide formation in the liver of rats. And also, this study dealt with an influence of scavengers on the hepatic lipid peroxide formation stimulated by PCB. Rats were given a 0.01% PCB diet supplemented with adequate nutrients, for 14 days. In an experiment, secobarbital was injected subcutaneously for the degradation of hepatic microsomal cytochrome P-450 heme. A marked liver enlargement and a significant increase of total liver lipid content were observed in the PCB group. The secobarbital enhanced the PCB-induced liver enlargement but no effect of secobarbital on the lipid content was recognized. PCB significantly induced hepatic microsomal cytochrome P-450, but not both cytochrome b5 and NADPH-cytochrome c reductase. The secobarbital suppressed the induction of cytochrome P-450 caused by PCB to approximately one-half. The hepatic vitamin A content significantly decreased on PCB administration and the secobarbital slightly enhanced the PCB-induced vitamin A reduction. However, the vitamin A content in the secobarbital-injected control group decreased to nearly the same levels as in the PCB groups. Therefore, it was presumed that the hepatic microsomal mixed function oxidase system, especially the cytochrome P-450, was possibly not directly involved in the PCB-induced hepatic vitamin A reduction or that a metabolic system related to mixed function oxidase system was involved in the reduction. On the other hand, the hepatic lipid peroxide content tended to increase on PCB administration though no significant difference was recognized. In contrast, the hepatic lipid peroxide content significantly increased in the secobarbital-injected PCB group as compared with the secobarbital-injected control group. However, there was no difference in the lipid peroxide contents between the control groups with and without the injection of secobarbital, and also between the PCB groups. The hepatic vitamin E contents lowered in the secobarbital-injected groups but no effect was observed on PCB administration. The glutathione peroxidase activity decreased significantly on PCB administration and the secobarbital further decreased the activity. Therefore, it was suggested that the significant increase and tendency of increase in hepatic lipid peroxide contents in the PCB groups with and without injection of secobarbital were ascribed to an insufficiency of lipid peroxide scavengers in the liver.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Effects of lipophilic derivatives of L-ascorbic acid and dehydro-L-ascorbic acid on the peroxidation of linoleic acid in neutral phosphate buffer containing alcohol.

6-O-Palmitoyl-AsA (AP) and -DHA (DHAP) suppressed LA peroxidation considerably in both 10% and 20% EtOH solutions. The duration of the suppression of LA peroxidation was longer with AP than with DHAP. But after the initial suppression of LA peroxidation, both derivatives showed an accelerating effect. 6-O-Acetyl-AsA (Ac-AsA) and -DHA (Ac-DHA) accelerated LA peroxidation from the start of the reaction in 10% EtOH, but suppressed it notably in 20% EtOH. 4-Phenyl-2,3-dihydroxy-2-buten-4-olide (PDHB) and 4-phenyl-2,3-dioxo-4-butenolide (PDOB) accelerated LA peroxidation in 10% EtOH. With 20% EtOH solution, PDHB suppressed LA peroxidation notably, as did AP, but PDOB showed only a short duration (about 1 h) of suppression. These results suggest the complexity of LA peroxidation catalyzed by lipophilic AsA or DHA in aqueous solution containing alcohol.

4-Butyrolactone↗
PubMed2002

Upregulation of vascular endothelial growth factor by hydrogen peroxide in human colon cancer.

AIM: To evaluate the effect of reactive oxygen species such as hydrogen peroxide on the progression of human colon cancer. METHODS: Human colon carcinoma cell lines, LS174T and HCT8, were treated respectively with 10(-5), 10(-7) or 10(-9) mol x L(-1) hydrogen peroxide for 24h,and co-cultured with human endothelial cell line ECV-304. The migration of ECV-304 induced by cancer cells was calculated and the expression level of vascular endothelial growth factor in cancer cells was determined by RT-PCR analysis and ELISA. Dactinomycin of 1.5mg x L(-1) which could block transcription of cancer cells was applied to observing the effects of H(2)O(2) on transcriptional activity and the relative half-life of VEGF mRNA. Finally,to evaluate the effect of H2O2 on NF-kappaB activity in colon cancer cells, NF-kappaB in cytoplasm and nucleus of the cells were detected with FITC-tagged antibody and its presence in the nucleus(Fn) vs cytoplasm(Fc) was monitored by measuring the green fluorescence integrated over the nucleus by laser scanning cytometry(LSC). RESULTS: Exogenouse hydrogen peroxide of low concentration increased the migration of endothelial cell induced by colon cancer cells. When cancer cells were treated with 10(-5) mol x L(-1) H2O2, the migration number of endothelial cells induced by LS174T cells was 203+/-70 and the number induced by HCT8 cells was 145+/-65. The two values were significantly higher than those treated with other concentrations of H2O2 (P<0.01). The expression of vascular endothelial growth factor in cancer cells, which could be blocked by dactinomycin, were increased to a certain degree, while the relative half-life of VEGF mRNA was not prolonged after treatment with hydrogen peroxide. The activity of NF-kappaB in colon cells rose after the cells were exposed to hydrogen peroxide for 24h. The Fn values in HCT8 cells were 91+/-13 (0 mol x L(-1) H2O2) and 149+/-40(10(-5) mol x L(-1) H2O2)(P<0.05), in LS174T cells were 127+/-35(0 mol x L(-1) H2O2) and 192+/-11(10(-5)mol x L(-1) H2O2) (P<0.05). It is similar to the case of VEGF expression in cancer cells. CONCLUSION: Hydrogen peroxide increases vascular endothelial growth factor expression in colon cancer cells, and it is likely that reactive oxygen species such as hydrogen peroxide facilitates the development of colon cancer.

Antioxidants↗
PubMed1985

Lipid peroxidation by bleomycin-iron complexes in vitro.

Lipid peroxidation catalyzed by bleomycin (BLM)-metal complexes was studied in vitro using arachidonic acid as the substrate. Iron complexes of BLM caused extensive lipid peroxidation, but other metal complexes did not. The lipid peroxidation caused by the iron complexes was inhibited by antioxidants such as dl-alpha-tocopherol, ascorbic acid etc., but not by other scavengers of hydroxyl and superoxide radicals, and of singlet oxygen. Cyanide ion suppressed the lipid peroxidation caused by BLM-Fe(II), but did not suppress the peroxidation activity of BLM-Fe(III). The peroxidation activity of BLM-Fe(II) was lost instantly by pre-incubation of the complex at 37 degrees C before mixing with arachidonic acid, but that of BLM-Fe(III) was not. These results indicate that the active form for the lipid peroxidation derived from BLM-Fe(II) differs from that of BLM-Fe(III).

Antioxidants↗
PubMed1992

Levels of plasma lipid peroxides before and after choledocholithotomy in patients with obstructive jaundice.

Plasma lipid peroxide levels were measured in a group of 40 healthy controls and 11 patients with jaundice. In the case of these 11 patients, we checked the plasma lipid peroxide concentrations prior to and after choledocholithotomy. Before choledocholithotomy, there were significantly higher mean concentrations of plasma lipid peroxides and bilirubin in patients with jaundice than in the control cases (11.8 +/- 2.3 vs. 2.0 +/- 0.1 nmol/ml and 10.3 +/- 1.82 vs. 0.7 +/- 0.03 mg/dl, respectively, P < 0.05). In addition, patients with jaundice had lower plasma vitamin E levels in comparison to the controls (8.2 +/- 0.6 vs. 12.2 +/- 0.5 micrograms/ml, P < 0.05). In patients with jaundice, the increased plasma lipid peroxides were clearly related to the serum levels of bilirubin (r = 0.87, P < 0.05). After surgery, the higher plasma levels of lipid peroxide and bilirubin were reduced markedly (11.8 +/- 2.3 vs. 3.7 +/- 0.4 nmol/ml and 10.3 +/- 1.82 vs. 3.1 +/- 0.47 mg/dl, respectively, P < 0.05) with the restoration of bile flow which was associated with improvement in liver function tests. Consequently, these results suggest that there is an involvement of lipid peroxidation in liver cells damaged by obstructive jaundice in patients with cholelithiasis, and that these high plasma lipid peroxide levels may correlate with the severity of the disease.

Adult↗
PubMed1999

In situ detection of lipid peroxidation by-products as markers of renal ischemia injuries in rat kidneys.

PURPOSE: Lipid peroxidation is an autocatalytic mechanism leading to oxidative destruction of cellular membranes. In renal transplantation, this mechanism is triggered by ischemia/reperfusion and may be of relevance in graft failure. MATERIALS AND METHODS: Using specific antibodies directed against malondialdehyde (MDA) and 4-hydroxynonenal (HNE) adducts, major aldehydic metabolites of lipid peroxidation, we investigated, in situ, by means of an immunohistochemical procedure, the occurrence of lipid peroxidation during different warm ischemic periods of 0, 15, 30, 45 and 60 minutes in rat kidneys prior to reperfusion. The same experiments included followup of the rats after nephrectomy and reperfusion for 10 days. RESULTS: We observed superficial and deep cortex immunostaining with both antibodies against MDA and HNE after 30 minutes of warm ischemia. This immunostaining was observed in the absence of any histological lesions, as assessed by routine staining. After 45 and 60 minutes of warm ischemia, lipid peroxidation byproducts were detected both in the cortex and in the medulla, which is associated with 33% and 66% of rat deaths respectively. CONCLUSIONS: This study confirms the involvement of the lipid peroxidation process in kidney damage during anoxia before reperfusion, and its extension to the whole organ. Lipid peroxidation byproducts were detectable in warm ischemic kidney, and the presence of medulla immunostaining was associated with the animals' death. Lipid peroxidation immunostaining might thus be useful as a sensitive tool to detect ischemic damage after warm ischemia prior to reperfusion, as well as in the decision to carry out kidney transplantation in humans.

Aldehydes↗
PubMed2001

Radiation induced peroxidative damage: mechanism and significance.

An interest has been generated in free radicals after the discovery of superoxide dismutase. These free radicals cause a number of diseases and are involved in the detrimental effect of ionizing radiation. Efforts have been made to understand their role in damage and death of the cell using lipid peroxidation process. Lipid peroxidation is an important effect of radiation on membranes, which apart from DNA, are critical targets of radiation action. This paper addresses the basic mechanism of radiation induced lipid peroxidation. Various factors, which determine the mode and magnitude of lipid peroxidation, are also discussed. Lipid peroxidation is shown to have importance in understanding the modifications of radiation effects. Efforts are made to show similarities between radiolytic and non-radiolytic lipid peroxidation. Recent findings related to the close link between radiation-induced lipid peroxidation and apoptosis are likely to open new avenues for future research and to develop new approaches for radiomodification of biological effects.

Animals↗
PubMed1998

Effect of long term bed rest in men on enzymatic antioxidative defence and lipid peroxidation in erythrocytes.

Bed rest is an integral part of treatment of numerous diseases. Typical examples are bone fractures of lower extremities and pelvis. Temporary immobilization is necessary also, e.g., in heart diseases (stroke), backbone and imminent abortion. The sick organism spares energy during the bed rest wich is beneficial. However, bed rest results in many alterations which are disadavantageous. They concern the function of almost all organs and systems but affect most significantly the locomotor and ciruclatory systems. Bed rest brings also about changes in the composition of peripheral blood and functions of the morphotic elements of blood. Red blood cells are subjected to the action of large amounts of reactive oxygen species (ROS). During oxidation of hemoglobin to methemoglobin superoxide radical anion (O2-) is formed: HbFe2+ + O2 --> MetHbFe3+ + O2- (1) Ferrous and ferric ions present in the cytoplasm of red blood cells may be catalysts of the Fenton reaction leading to the production of the hydroxyl radical: O2- + Fe3+ --> O2- + Fe2+ (2) Fe2+ + H2O2 --> Fe3+ + OH + HO- (3) OH shows a tremendous reactivity. It may react with lipids, proteins, nucleic acids and carbohydrates. The process of lipid peroxidation is best understood. It concerns mainly polyunsaturated fatty acids present in cell membranes. Peroxidation of membrane lipids decreases membrane fluidity and impairs its barrier function. The lowered membrane fluidity compromises erythrocyte deormability which in turn disturbs oxygen delivery to the tissues. End productions of lipid peroxidation are low-molecular wieght compounds, among them carbohydrates (ethane and pentane) and aldehydes, e.g. malondialdehyde (MDA). MDA concentration is an acknowldeged marker of the intensity of lipid peroxidation. Erythrocytes contain a complex system of protection against the action of ROS. It includes various enzymatic and non-enzymatic mechanism. The most important antioxidative enzymes of the red blood cells are superoxide dismutase (Cu,Zn-SOD, EC 1.15.1.1) catalase (CAT, EC 1.11.1.6) and glutathione peroxidase (GSH-Px, EC 1.11.1.9). Cu,Zn-SOD catalyzes the dismuation of O2- to hydrogen peroxide (H2O2). Catalase and peroxidase remove H2O2 and, moreover, GSH-Px can reduce lipid peroxides. Under normal conditions an equilibrium exists between the formation and removal ROS. If ROS are formed in excess or the defensive antioxidative mechanism are inefficient, oxidative stress develops. Derangement of the equilibrium between the formation and removal of ROS is important in the pathosgenesis of many diseases, e.g. atherosclerosis, diabetes, Down syndrome and Alzheimer disease. There are literature data on disturbances of enzymatic antioxidant defense mechanism of blood plateless during bed rest. This study was aimed at an examination of the post-traumatic bed rest on the enzymatic antioxidative defense mechanisms and lipid peroxidation in erythrocytes.

Adult↗
PubMed1979

Effects of lipid peroxidation on the activity of microsomal UDPglucuronosyltranserase.

This study is concerned with effects of lipid peroxidation of liver microsomal fractions in vitro on the activity of the membrane-dependent enzyme UDPglucuronosyltransferase. Peroxidation was initiated by the ascorbate-Fe2+ redox couple. Peroxidation had a biphasic effect on transferase activity (with p-nitrophenol or o-aminophenol as acceptors). An initial activation at low levels of peroxidation was followed by inactivation after more prolonged peroxidation. Activation was more pronounced with rat preparations than with those from guinea pig. When taken in conjunction with previous work on the effects of membrane perturbants on transferase activity the results indicate that activation was the result of membrane perturbation, probably resulting from shortening of phospholipid hydrocarbon chains. The inactivation of the enzyme in guinea pig liver microsomal preparations was not reversed by adding phospholipids. It is concluded that the irreversible inactivation was probably due to chemical reaction of intermediate products of peroxidation with essential membrane components, possibly the enzyme itself. Further experiements suggested that lipid peroxides were responsible.

Animals↗
PubMed2002

[Upregulation of vascular endothelial growth factor by peroxide in human colon cancer].

OBJECTIVE: To clarify the possible effect of reactive oxygen species such as hydrogen peroxide on progression of human colorectal cancer. METHOD: Human colon carcinoma cell lines, L174T and HCT8, were treated with low concentration of hydrogen peroxide (10(-5) mol/L, 10(-7) mol/L and 10(-9) mol/L, possessed no effect on cancer cell growth) for 24 hours before being co-cultured with human endothelial cell line ECV-304. The migration of ECV-304 induced by cancer cells was calculated and the expression of vascular endothelial growth factor (VEGF) in cancer cells was determined using RT-PCR and ELISA. Dactinomycin (1.5 microg/ml) was applied to block the transcription of cancer cell so as to observe the effect site of cell. Finally the activity of NF-KappaB of cancer cells was estimated using laser scanning cytometry. RESULTS: Exogenous hydrogen peroxide of low concentration promoted the migration of endothelial cell induced by colon cancer cell. When the concentration of H(2)O(2) was 10(-5) mol/L, the average number of migration of endothelial cell induced by LS174T was 202.6 +/- 70.2, higher than the value of 154.6 +/- 37.9 when no H(2)O(2) was given (t = 3.4751, P = 0.0083). When the concentration of H(2)O(2) was 10(-5) mol/L, the average number of migration of endothelial cell induced by HCT8 was 145.4 +/- 65.3, higher than the value of 113 +/- 72.7 when no H(2)O(2) was given (t = 4.4183, P = 0.0084). The expression of vascular endothelial growth factor in cancer cells was enhanced to a certain degree, which could be blocked by Dactinomycin. And the half-time of VEGF mRNA was not prolonged by treatment with hydrogen peroxide. The activity of NF-KappaB of both colon carcinoma cell lines was at a higher level after being treated with hydrogen peroxide for 24 hours. CONCLUSION: Hydrogen peroxide increases vascular endothelial growth factor expression in colon cancer cell, and it is possible that such reactive oxygen species as hydrogen peroxide facilitates development of colon cancer.

Colonic Neoplasms↗