Lipid Peroxidation In Rat Tissues Research Articles

In Vitro Antioxidant Activity and Effect of Parkia biglobosa Bark Extract on Mitochondrial Redox Status

Aqueous-methanolic extract of Parkia biglobosa bark (PBB) was screened for its polyphenolic constituents, in vitro antioxidant activity, and effect on mitochondria redox status. The in vitro antioxidant activity was assessed by using the scavenging abilities and the reducing powers of 1,1-diphenyl-2-picrylhydrazyl radical (DPPH) and 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) diammonium salt radical cation against Fe3+. Subsequently, the ability of PBB to inhibit lipid peroxidation induced by FeSO4 (10 μm) and its metal-chelating potential were investigated. The effects of the extract on basal reactive oxygen species (ROS) generation and on the mitochondrial membrane potential (ΔΨm) in isolated mitochondria were determined by using 2′, 7′-dichlorodihydrofluorescin (DCFH) oxidation and safranin fluorescence, respectively. PBB mitigated the Fe(II)-induced lipid peroxidation in rat tissues and showed dose-dependent scavenging of DPPH (IC50: 98.33 ± 10.0 μg/mL) and ABTS. (trolox equivalent antioxidant concentration, TEAC value = 0.05), with considerable ferric-reducing and moderate metal-chelating abilities. PBB caused slight decreases in both the liver and the brain mitochondria potentials and resulted in a significant decrease (p < 0.001) in DCFH oxidation. Screening for polyphenolics using high-performance liquid chromatography coupled to a diode array detector (HPLC-DAD) revealed the presence of caffeic acid, gallic acid, catechin, epigalocatechin, rutin, and quercetin. These results demonstrate for the first time the considerable in vitro antioxidant activity and favorable effect of PBB on mitochondria redox status and provide justification for the use of the plant in ethnomedicine.

Antioxidant activities of licorice-derived prenylflavonoids

Glycyrrhiza uralensis (or licorice) is a widely used Oriental herbal medicine from which the phenylflavonoids dehydroglyasperin C (DGC), dehydroglyasperin D (DGD), and isoangustone A (IsoA) are derived. The purpose of the present study was to evaluate the antioxidant properties of DGC, DGD, and IsoA. The three compounds showed strong ferric reducing activities and effectively scavenged DPPH, ABTS+, and singlet oxygen radicals. Among the three compounds tested, DGC showed the highest free radical scavenging capacity in human hepatoma HepG2 cells as assessed by oxidant-sensitive fluorescent dyes dichlorofluorescein diacetate and dihydroethidium bromide. In addition, all three compounds effectively suppressed lipid peroxidation in rat tissues as well as H2O2-induced ROS production in hepatoma cells. This study demonstrates that among the three phenylflavonoids isolated from licorice, DGC possesses the most potent antioxidant activity, suggesting it has protective effects against chronic diseases caused by reactive oxygen species as well as potential as an antioxidant food additive.

Effects of methiocarb on lipid peroxidation in rat tissues

Effects of methiocarb on lipid peroxidation in rat tissues

Protective effects of GH and IGF-I against iron-induced lipid peroxidation in vivo

Iron overload may enhance oxidative damage. Growth hormone (GH) and insulin-like growth factor-I (IGF-I) are involved in oxidative processes, lipid peroxidation (LPO) included. The aim of the study was to evaluate the in vivo effects of GH, IGF-I and/or iron on LPO in rat tissues. Male Wistar rats were administered iron (Fe 2+; 3 mg/100 g b.w., i.p., on the 8th day) and/or GH (0.2 IU/100 g b.w.), and/or IGF-I (2 μg/100 g b.w.) once daily for 8 days. LPO products (malondialdehyde+4-hydroxyalkenals) were measured in rat brain, lung, small intestine, liver, kidney, testis, spleen and serum. Iron injection increased LPO only in the small intestine and that effect was completely prevented by either GH or IGF-I. In the brain, GH decreased, whereas IGF-I increased, the basal LPO. GH and IGF-I possess some ability to prevent iron-induced oxidative damage in iron sensitive tissues, but contribute to oxidative imbalance in other tissues.

Positive influence of Centchroman on cardiovascular system and tissue lipid peroxidation in rats

Background Centchroman, a nonsteroidal oral contraceptive, was evaluated for its hitherto unstudied effect on cardiovascular system, thyroid function and tissue lipid peroxidation in rats. Study Design Wistar sperm-positive female rats were treated with Centchroman (1.5 mg/kg per day, po) for 10 days and the alterations in serum concentration of thyroid hormones [triiodothyronine (T 3) and thyroxine (T 4)], insulin, glucose, total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), triglycerides (TG), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phospahatase (ALP) activity, hepatic type-1 iodothyronine 5′-monodeiodinase (5′D) enzyme activity and hepatic, renal, cardiac and serum lipid peroxidation (LPO) were studied. Simultaneously, alterations in endogenous antioxidants [superoxide dismutase (SOD); catalase (CAT) and reduced glutathione (GSH)], relative risk ratio (RR), atherogenic index (AI) and daily rate of food and water consumption were also investigated as supportive parameters. Results Centchroman administration resulted in the complete inhibition of pregnancy. It increased serum T 4 marginally and HDL-C levels, hepatic SOD, CAT and GSH; cardiac SOD and GSH and renal SOD and CAT activity significantly. However, it reduced LPO in all tissues; concentrations of other serum lipids; AI; RR and activity of ALP. Conclusions As Centchroman administration did not alter the concentrations of most active thyroid hormone, T 3, serum insulin and glucose, it appears that the drug has no side effect on thyroid function and glucose metabolism. Rather, it possesses cardiovascular and anti-peroxidative benefits.

Cholesterol as target of Fe–NTA-induced lipid peroxidation in rat tissues

Intraperitoneal injection of the iron–chelate, ferric–nitrilotriacetate (Fe–NTA), induces renal proximal tubular damage associated with oxidative damage in vivo. A sub-lethal dose of Fe–NTA (15 mg Fe/kg body weight) was administered IP to rats; animals were sacrificed and liver, kidney and plasma were collected 1–4 h after injection. In response to the Fe–NTA administration, there were significant time-dependent reductions of the levels of total lipids, cholesterol and total unsaturated fatty acids, and a rise in the concentrations of conjugated dienes, 7-ketocholesterol and fatty acids hydroperoxides, showing a pattern inversely correlated in plasma, kidney and liver. Cholesterol level decreased significantly from 1 h after injection in the kidney and 3–4 h in the plasma and liver of treated rats. This is the first report on cholesterol reduction and accumulated 7-ketocholesterol in the tissues of rats treated with Fe–NTA as a consequence of lipid peroxidation.

Protective effect of capsinoid on lipid peroxidation in rat tissues induced by Fe-NTA

The activity of a single IP administration (15 or 30 mg/Kg body weight) of vanillyl nonanoate, a simplified analog of capsiate, on ferric nitrilotriacetate (Fe-NTA)-mediated oxidative damage was investigated. A sub-lethal dose of Fe-NTA (15 mg Fe/Kg body weight) was administered IP to rats; animals were sacrificed, and kidney and plasma were collected 1 h after injection. In response to the Fe-NTA administration, a reduction of the levels of total lipids, total unsaturated fatty acids and cholesterol was observed, accompanied by a rise in the concentrations of malondialdehyde (MDA), conjugated dienes fatty acids hydroperoxides and 7-ketocholesterol in plasma and kidney 1 h after administration. A pre-treatment with synthetic capsiate (SCPT) showed remarkable protective effect on the reduction of the levels of total lipids, total unsaturated fatty acids and cholesterol, and the cellular antioxidant vitamin E, inhibiting the increase of MDA, conjugated dienes fatty acids hydroperoxides and 7-ketocholesterol in the plasma and kidney. The protective effect of SCPT and two analogues (vanillyl alcohol and vanillin) during the linoleic acid and cholesterol oxidation was investigated in in vitro systems, providing evidence of definite structure–activity relationships.

Diminution of tissue lipid peroxidation in rats is related to the in vitro antioxidant capacity of wine

Wine polyphenols could reinforce the endogenous antioxidant system, thereby diminishing oxidative damage. Studies in chronic models to understand the relationship between the bioavailability of polyphenols and their biological effects are still lacking. The aim of the present study was to prove the hypothesis that the antioxidant capacity of wines in vitro is positively correlated with the antioxidant capacity of plasma and negatively correlated with tissue lipid peroxidation, after chronic wine consumption. Adult rats received: water (control group), wine having variable phenolic content, ethanol (12.5% v/v) or alcohol-free red wine, for 4 weeks. The antioxidant capacity of wines in vitro and that of plasma induced in vivo were assessed through the reduction of ferric iron (FRAP, ferric reducing ability of plasma). Lipid peroxidation (production of thiobarbituric acid reactive substances, TBARS), and the activity of the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), were determined in kidney, liver and lung. The phenolic content of wines was positively correlated with their FRAP values in vitro (r = 0.407, p < 0.002). Also, the relationship between wine FRAP in vitro to its respective plasma value in vivo showed a positive correlation (r = 0.433, p < 0.005). Phenolic concentration of wine did not influence the activity of CAT, SOD and GSH-Px of the three organs studied, but it was negatively correlated with their production of TBARS (r = −0.852, −0.891 and −0.790 for kidney, liver and lung, respectively, p < 0.001). The present data provide evidence that the antioxidant capacity of wine in vitro implicates a homologous effect in vivo, thus helping to modulate tissue lipid peroxidation.

Effect of cadmium and aluminum intake on the antioxidant status and lipid peroxidation in rat tissues.

This work aimed to study the relationship between the accumulation of cadmium (Cd) or aluminum (Al) in certain tissues and the levels of lipid peroxides as well as tissue antioxidants. To carry out such investigations, CdCl2 was given to rats in two dose levels; 0.5 or 2.0 mg/kg i.p for 1 day or daily repeated doses for 2 weeks. Al was given as AlCl3 either in a single dose of 100 mg/kg or daily repeated doses of 20 mg/kg for 2 and 4 weeks. The measured parameters were tissue malondialdehyde (MDA, index of lipid peroxidation) and reduced glutathione (GSH) levels as well as the activities of glutathione peroxidase (GSH-PX), glutathione reductase (GSSG-R), and glucose-6-phosphate dehydrogenase (G-6-PDH) enzymes. Liver and kidney functions were assessed by measuring serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities as well as serum urea and creatinine concentrations. Cd and Al concentrations in the studied tissues were also measured. Results indicated that tissue Cd was significantly increased after administration of either Cd doses. After a single dose of 0.5 or 2.0 mg/kg CdCl2, the increase in tissue Cd levels were accompanied by an increase in MDA and a decrease in GSH levels. On the other hand, after repeated administration of Cd, tissue Cd accumulation was accompanied by increased hepatic and renal GSH levels with decrease in MDA content and a decrease in GSH-PX activity in liver. Liver function was affected at all dose regimens, whereas kidney function was affected only after 2 weeks administration of the higher dose. In Al treated rats, Al concentration was shown to be increased in liver much more than in brain. This was accompanied by a slight decrease in hepatic GSH level after 2 weeks and a decrease in GSH-PX activity after 4 weeks. Liver function was affected only after repeated injection of Al for 2 or 4 weeks. In general, Al administration exhibited safer pattern than Cd.

Effect of Cadmium and Aluminum Intake on the Antioxidant Status and Lipid Peroxidation in Rat Tissues

This work aimed to study the relationship between the accumulation of cadmium (Cd) or aluminum (Al) in certain tissues and the levels of lipid peroxides as well as tissue antioxidants. To carry out such investigations, CdCl2 was given to rats in two dose levels; 0.5 or 2.0 mg/kg i.p for 1 day or daily repeated doses for 2 weeks. Al was given as AlCl3 either in a single dose of 100 mg/kg or daily repeated doses of 20 mg/kg for 2 and 4 weeks. The measured parameters were tissue malondialdehyde (MDA, index of lipid peroxidation) and reduced glutathione (GSH) levels as well as the activities of glutathione peroxidase (GSH-PX), glutathione reductase (GSSG-R), and glucose-6-phosphate dehydrogenase (G-6-PDH) enzymes. Liver and kidney functions were assessed by measuring serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities as well as serum urea and creatinine concentrations. Cd and Al concentrations in the studied tissues were also measured. Results indicated that tissue Cd was significantly increased after administration of either Cd doses. After a single dose of 0.5 or 2.0 mg/kg CdCl2, the increase in tissue Cd levels were accompanied by an increase in MDA and a decrease in GSH levels. On the other hand, after repeated administration of Cd, tissue Cd accumulation was accompanied by increased hepatic and renal GSH levels with decrease in MDA content and a decrease in GSH-PX activity in liver. Liver function was affected at all dose regimens, whereas kidney function was affected only after 2 weeks administration of the higher dose. In Al treated rats, Al concentration was shown to be increased in liver much more than in brain. This was accompanied by a slight decrease in hepatic GSH level after 2 weeks and a decrease in GSH-PX activity after 4 weeks. Liver function was affected only after repeated injection of Al for 2 or 4 weeks. In general, Al administration exhibited safer pattern than Cd. © 2001 John Wiley & Sons, Inc. J Biochem Mol Toxicol 15:207–214, 2001

Mechanism of biochemical action of substituted 4-Methylbenzopyran-2-ones. Part 3: A novel mechanism for the inhibition of biological membrane lipid peroxidation by dioxygenated 4-Methylcoumarins mediated by the formation of a stable ADP-Fe-Inhibitor mixed ligand complex

7,8-Dihydroxy-4-methylcoumarin (DHMC) and 7,8-diacetoxy-4-methylcoumarin (DAMC) have been reported to effectively inhibit in-vivo lipid peroxidation in rat tissues induced by CCl 4 and paraquat. DHMC was found to readily impart green colour to the lipid peroxidation incubation mixture containing ADP and Fe 3+, whereas DAMC formed green complex only upon incubation with liver microsomes, confirming our earlier observation that liver microsomal deacetylase hydrolyses DAMC to DHMC. Sensitive pH metric technique revealed the formation of ADP-Fe-DHMC ternary complex with highest stability, while Fe-DHMC and ADP-DHMC had negligible stabilities concluding that ADP-perferryl ion formation is prevented by DHMC resulting in the production of stable ternary mixed ligand complex (ADP-Fe-DHMC), thereby inhibiting the formation of O 2 −., and eventually other reactive oxygen species (ROS) responsible for membrane lipid peroxidation.

The effect of duration of compression on lipid peroxidation after experimental spinal cord injury.

The present study was performed to evaluate the effect of duration of acute spinal cord compression on tissue lipid peroxidation in rats. A clip compression method (1) was used to produce acute spinal cord injury. Rats were divided into 3 groups, each consisting of 10. At 1 hour after trauma all rats were sacrificed, and MDA content of the injured spinal cord segment was measured. The tissue MDA contents were 3.922 mumolMDA/gww in group 1 (control), 10.192 mumol MDA/gww in group 2 (30 seconds compression), and 12.147 mumolMDA/gww in group 3 (60 seconds compression). These results demonstrate that the length of duration of compression significantly enhances lipid peroxidation. Our study supported the view that persisting compression may cause progression of secondary mechanisms which may irreversibly eliminate any potential for recovery.

Effect of ubiquinone on exercise-induced lipid peroxidation in rat tissues.

Changes in the amount of thiobarbituric acid-reactive substances (TBARS), an index of the lipid peroxidation, were estimated in liver, heart, and the red and white components of gastrocnemius muscle of control (C) and ubiquinone-treated rats (T, 10 mg.kg-1 daily, for 4 weeks) at rest, and 3 and 24 h after running until the rats were exhausted. The activity of creatine kinase in serum and the level of the non-protein sulphhydryl groups (NP-SH) in the above organs were also determined. The running time until exhaustion was longer in T than in C [83.0 (SD 13.8) vs 72.2 (SD 14.8) min, P < 0.05]. The exercise resulted in a significant increase (P < 0.01) in the TBARS amounts in all the tissues obtained from C and in the liver and heart of T. The postexercise amounts of TBARS were significantly higher (P < 0.01) in C than in T. The resting amounts of NP-SH in the heart and liver were significantly higher (P < 0.05) in C compared to T. The exercise led to a decrease in the NP-SH content in the heart and liver (P < 0.05) of C but did not seem to affect the NP-SH contents in these tissues in T. No effect of ubiquinone treatment on postexercise increase in the serum creatine kinase concentration was found. It was concluded that in rats ubiquinone treatment markedly suppresses exercise-induced lipid peroxidation in such organs as liver, heart and gastrocnemius muscle.

Effects of dietary fats and benzo[a]pyrene on lipid peroxidation in rat tissues

Effects of dietary fats and benzo[a]pyrene on lipid peroxidation in rat tissues

Arsenic increased lipid peroxidation in rat tissues by a mechanism independent of glutathione levels.

The role of lipid peroxidation in the mechanism of arsenic toxicity was investigated in female rats pretreated with N-acetylcysteine (NAC, a glutathione [GSH] inducer) or with buthionine sulfoximine (BSO, a GSH depletor). Rats were challenged with sodium arsenite, and sacrificed 1 hr after this treatment. Results showed that arsenic decreased GSH levels and increased lipid peroxidation in liver, kidney, and heart, with a larger effect at 18.2 mg/kg than at 14.8 mg/kg for lipid peroxidation induction. In the liver of rats treated with arsenic, pretreatment with NAC increased the levels of GSH and decreased lipid peroxidation. In kidney and heart, NAC pretreatment protected the tissues against arsenic-induced depletion of GSH levels, but the same degree of protection was not found for lipid peroxidation induction. In its turn, BSO had an additive effect with arsenic in lowering the levels of GSH in the liver and kidney, but an inverse correlation between GSH levels and lipid peroxidation was found only in liver. Arsenic content in tissues of rats pretreated with NAC was lower than in rats treated only with arsenic. In rats with depleted levels of GSH (BSO-pretreated rats), a shift in arsenic tissue distribution was found, with higher levels in skin and lower levels in kidney. A clear tendency for a positive correlation between arsenic concentration and lipid peroxidation levels was found in liver, kidney, and heart.

Arsenic Increased Lipid Peroxidation in Rat Tissues by a Mechanism Independent of Glutathione Levels

Arsenic Increased Lipid Peroxidation in Rat Tissues by a Mechanism Independent of Glutathione Levels

Degree of Protein Deficiency Affects the Extent of the Depression of the Antioxidative Enzyme Activities and the Enhancement of Tissue Lipid Peroxidation in Rats

To investigate the effects of various dietary protein levels on tissue lipid peroxidation and antioxidative enzyme activities, four groups of Long-Evans male weanling rats were fed a 6, 8, 12 or 20% lactalbumin diet for 6 wk. The red blood cell in vitro spontaneous hemolysis values were 28.6, 24.9, 18.9 and 14.1% for the rats fed the 6, 8, 12 and 20% lactalbumin diets, respectively. The thiobarbituric acid-reactive substances (TBARS) in plasma, RBC, liver, kidney, muscle, lung, spleen and heart were lowest in the group fed the 20% lactalbumin diet. Rats fed the diet containing 12% lactalbumin had significantly greater TBARS in plasma, spleen, kidney and muscle compared with rats fed the 20% lactalbumin diet. Rats fed the 8% lactalbumin diet had markedly higher TBARS levels (P < 0.05) in all tissues examined than did those fed the 12% lactalbumin diet. The TBARS in all eight tissues of the rats fed the 6% lactalbumin diet were even higher than those of rats fed the 8% lactalbumin diet (P < 0.05). The activities of glutathione peroxidase, superoxide dismutase and glucose-6-phosphate dehydrogenase in RBC were gradually lowered (P < 0.05) when the dietary protein level was decreased stepwise. The activities of these antioxidative enzymes in liver also were reduced significantly when dietary protein level decreased from 20 to 12% and then to 8%. These enzyme activities in the rats fed the diet containing 6% lactalbumin generally were not different from those of the rats fed 8% lactalbumin.(ABSTRACT TRUNCATED AT 250 WORDS)

Vitamin A Inhibits Doxorubicin-Induced Membrane Lipid Peroxidation in Rat Tissues in Vivo

The antioxidant activity of vitamin A against lipid peroxidation induced by doxorubicin in rat tissues in vivo was investigated. A single ip injection of doxorubicin (30 mg/kg body wt) markedly raised the level of peroxidated lipids measured as TBARS and conjugated dienes in heart and brain membrane preparations. Other tissues, such as retina and liver, did not show any increase of lipid peroxides over control values. Pretreatment of rats with two daily subcutaneous injections of retinol palmitate (0.25 g/kg body wt), for 2 days, before injecting doxorubicin, inhibited peroxidation of heart and brain membrane lipids. The antioxidant action of vitamin A does not appear to be mediated by enhancement of antioxidant enzyme activities committed to detoxify oxygen radicals. Superoxide dismutase and catalase, measured in heart and brain cytosol, were not affected by the vitamin A treatment. On the contrary, a slight increase of catalase activity was observed in heart and brain cytosol from rats that had been treated with doxorubicin. Excess vitamin A may be localized in membranes. Appreciable increase of retinyl esters and retinol was measured in membrane preparations from rats that had been treated with vitamin A, with respect to control animals. Brain and heart membrane preparations from rats receiving vitamin A, assayed in vitro in the presence of an Fe3+ ascorbate induction system, showed a delay at the beginning of the lipid peroxidation and generated lesser amounts of TBARS, with respect to membranes from control rats. Thus, the increase of vitamin A within cell membranes results in an increased resistance of membrane lipids to peroxidation, both endogenously produced and induced in vitro. These results may be consistent with the hypothesis that vitamin A may act as a physiological antioxidant in cell membranes where it is localized.

Studies on lipid peroxidation in rat tissues following administration of low and moderate doses of cadmium chloride

The susceptibility to lipid peroxidation (LPO) of liver, kidneys, brain, lungs, heart, and testes was assessed in rats administered intraperitoneally with various doses of cadmium (Cd). Dose-response studies were carried out with male Long Evans rats (12-week-old; 300 ± 33 g) injected with 25, 125, 500, and 1250 μg Cd/kg as CdCl 2 and sacrificed after 24 h. In time-response studies, animals were administered with 25 and 500 μg Cd/kg as CdCl 2 and sacrificed after 2, 6, 12, 24, and 72 h. Exposure of rats to low and moderate doses of Cd by the intraperitoneal route stimulated LPO in all the tissues investigated as assessed by the measurement of thiobarbituric acid reactive substances (TBARS). Lungs and brain were the most responsive, and these tissues and liver displayed early responses following Cd exposure. Comparison of LPO to various tissue indicators (for liver: alanine aminotransferase (ALT), sorbitol dehydrogenase (SDH), alkaline phosphatase (ALP); for lungs: ALP, gamma-glutamyl transpeptidase (GGT)) suggested that low doses of Cd stimulated LPO without any evidence of acute damages. These results suggest that LPO is an early and sensitive consequence of Cd exposure as determined in various organs. Investigation of liver, lungs, and heart antioxidant defense system components (glutathione peroxidase (GPX), glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PDH), superoxide dismutase (SOD)) revealed that GPX might be considered as a potential modulator of the Cd-induced LPO reaction in lungs and heart tissues.

Platelet function and tissue lipid peroxidation in rats fed polyunsaturated fatty acids

Platelet function and tissue lipid peroxidation in rats fed polyunsaturated fatty acids