Pulmonary and hepatic glutathione levels, glutathione shuttle enzymes and lipid peroxidation in rats exposed intratracheally to coal fly ash

Fly ash and fly ash residue increased the formation of conjugated dienes and the levels of oxidized glutathione (GSSG) and reduced the levels of reduced glutathione (GSH) in lung and liver whereas fly ash extract administration had no effect on the formation of conjugated dienes and glutathione levels in lung and liver. Fly ash and fly ash residue reduced the activity of glutathione reductase both in lung and liver but did not alter the activity of glutathione peroxidase. Fly ash and fly ash extract significantly increased glucose-6-phosphate dehydrogenase activity in lung whereas in liver, fly ash and fly ash residue reduced the activity of glucose-6-phosphate dehydrogenase. Fly ash residue did not alter the activity of glucose-6-phosphate dehydrogenase in lung whereas fly ash extract was not effective in liver.     

The effect of lipoic acid on antioxidant status and lipid peroxidation in rats exposed to chronic restraint stress

This study was designed to investigate effect of alpha-lipoic acid (LA) on lipid peroxidation, nitric oxide production and antioxidant systems in rats exposed to chronic restraint stress. Twenty four male Wistar rats, aged three months, were divided into four groups: control (C), the group treated with LA (L), the group exposed to restraint stress (S) and the group exposed to stress and treated with LA (LS). Restraint stress was applied for 21 days (1 h/day) and LA (100 mg/kg/day) was injected intraperitonally to the L and LS groups for the same period. Restraint stress significantly decreased brain copper/zinc superoxide dismutase (Cu,Zn-SOD) and brain and retina glutathione peroxidase (GSH-Px) and catalase (CAT) activities compared with the control group. Thiobarbituric acid reactive substances (TBARS), nitrite and nitrate levels were significantly increased in the tissues of the S group compared with the C group. LA produced a significant decrease in brain and retina TBARS, nitrite and nitrate levels of the L and LS groups compared to their corresponding control groups. LA increased all enzyme activities in the tissues of the LS group compared to the S group. Our study indicated that LA is an ideal antioxidant candidate for the prevention of stress-induced lipid peroxidation.     

Effect of riboxine on processes of lipid peroxidation and activity of antioxidant enzymes in thymocytes of rats with radiation injury

The disorders of oxidative homeostasis with accumulation of lipid peroxidation products upon depletion of functional capacity of antioxidant defense in thymus lymphocytes after irradiation in doses of 1.0 and 7.78 Gy were shown. The riboxine injection leads to normalization of balance in prooxidant-antioxidant system (with a decrease of formation of lipid peroxidation and activation of antioxidant enzyme system) in early terms after X-ray exposure.     

Activity of glutathione peroxidase, glutathione reductase, and lipid peroxidation in erythrocytes in workers exposed to lead

The aim of this study was to estimate the activity of glutathione peroxidase (GPx), glutathione reductase (GR), and malondialdehyde (MDA) in erythrocytes in healthy male employees of zinc and lead steelworks who were occupationally exposed to lead over a long period of time (about 15 yr). Workers were divided into two subgroups: the first included employees with low exposure to lead (LL) (n=75) with blood lead level PbB=25–40 μg/dL and the second with high exposure to lead (HL) (n=62) with PbB over 40 μg/dL. Administration workers (n=35) with normal levels of PbB and zinc protoporphyrin in blood (ZPP) in blood were the control group. The activity of GPx significantly increased in LL when compared to the control group (p<0.001) and decreased when compared to the HL group (p=0.036). There were no significant changes in activity of GR in the study population. MDA erythrocyte concentration significantly increased in the HL group compared to the control (p=0.014) and to the LL group (p=0.024). For the people with low exposure to lead (PbB=25–40 μg/dL), the increase of activity of GPx by about 79% in erythrocytes prevented lipid peroxidation and it appears to be the adaptive mechanism against the toxic effect of lead. People with high exposure to lead (with PbB over 40 μg/dL) have shown an increase in MDA concentration in erythrocytes by about 91%, which seems to have resulted from reduced activity of GPx and the lack of increase in activity of GR in blood red cells.     

Changes in photosynthesis, antioxidant enzymes and lipid peroxidation in soybean seedlings exposed to UV-B radiation and/or Cd

Aims

With a high growth rate and biomass production, bamboos are frequently used for industrial applications and recently have proven to be useful for wastewater treatment. Bamboos are considered as Si accumulators and there is increasing evidence that silicon may alleviate abiotic stresses such as metal toxicity. The aim of this study was to investigate the extent of metal concentrations and possible correlations with Si concentrations in plants.

Methods

This study presents, for the first time, reference values for silicon (Si), copper (Cu) and zinc (Zn) concentrations in stems and leaves of various bamboo species grown under the natural pedo-climatic conditions of the island of Réunion (Indian Ocean).

Results

A broad range of silicon concentrations, from 0 (inferior to detection limit) to 183 mg g^?1 dry matter (DM), were found in stems and leaves. Mean leaf Cu and Zn concentrations were low, i.e. 5.1 mg kg^?1 DM and 15.7 mg kg^?1 DM, respectively. Silicon, Cu and Zn concentrations increased over the following gradient: stem base?<?stem tip?<?leaves. Significant differences in Si, Cu and Zn contents (except Zn in the stem) were noted between bamboo species, particularly between monopodial and sympodial bamboo species, which differ in their rhizome morphology. Sympodial bamboos accumulated more Si and Cu than monopodial bamboos, in both stems and leaves, whereas sympodial bamboos accumulated less Zn in leaves than monopodial bamboos.

Conclusions

The findings of this study suggest that a genotypic character may be responsible for Si, Cu and Zn accumulation in bamboo.     

Region specific increase in the antioxidant enzymes and lipid peroxidation products in the brain of rats exposed to lead

The objective of this study is to determine the effect of lead (pb) on antioxidant enzymes and lipid peroxidation products in different regions of rat brain. Wistar male rats were treated with lead acetate (500 ppm) through drinking water for a period of 8 weeks. Control animals were maintained on sodium acetate. Treated and control rats were sacrificed at intervals of 1st, 4th and 8th week and the whole brains were dissected on ice into four regions namely the cerebellum, the hippocampus, the frontal cortex and the brain stem. Antioxidant enzymes namely catalase and superoxide dismutase in all the four regions of brain were determined. In addition, lipid peroxidation products were also estimated. The results indicated a gradual increase in the activity of antioxidant enzymes in different regions of the brain and this response was time-dependent. However, the increase was more in the cerebellum and the hippocampus compared to other regions of the brain. The lipid peroxidation products also showed a similar trend suggesting increased effect of lead in these two regions of the brain. The data indicated a region-specific oxidative stress in the brain exposed to lead.     

Age-related changes in antioxidant enzyme activities and lipid peroxidation in lungs of control and sulfur dioxide exposed rats

Antioxidant defenses within the lung are pivotal in preventing damage from oxidative toxicants. There have also been several reports with conflicting results on the antioxidant system during aging. In this study, we attempted to investigate age-related alterations in both antioxidant enzyme activities and thiobarbituric acid-reactive substances (TBARS), a product of lipid peroxidation, in the whole lung of control and sulfur dioxide (SO₂) exposed rats of different age groups (3-, 12-, and 24-months-old). Swiss-Albino Male rats were exposed to 10 ppm SO₂ 1 hr/day, 7 days/week for 6 weeks. The antioxidant enzymes examined include Cu,Zn-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione S-transferase (GST). A mixed pattern of age-associated alterations in antioxidant activities was observed. SOD, GSH-Px and GST activities were increased with age, but CAT activity was decreased. Lung SOD, GSH-Px and GST activities were also increased in response to SO₂. The level of TBARS was increased with age. SO₂ exposure stimulated lipid peroxide formation in the lung as indicated by an increase in the level of TBARS. These findings suggest that both aging and SO₂ exposure may impose an oxidative stress to the body. We conclude that the increase in the activities of the antioxidant enzymes of the lung during aging, could be interpreted as a positive feedback mechanism in response to rising lipid peroxidation.     

Age-related changes in antioxidant enzyme activities and lipid peroxidation in lungs of control and sulfur dioxide exposed rats

Antioxidant defenses within the lung are pivotal in preventing damage from oxidative toxicants. There have also been several reports with conflicting results on the antioxidant system during aging. In this study, we attempted to investigate age-related alterations in both antioxidant enzyme activities and thiobarbituric acid-reactive substances (TBARS), a product of lipid peroxidation, in the whole lung of control and sulfur dioxide (SO₂) exposed rats of different age groups (3-, 12-, and 24-months-old). Swiss-Albino Male rats were exposed to 10 ppm SO₂ 1 hr/day, 7 days/week for 6 weeks. The antioxidant enzymes examined include Cu,Zn-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione S-transferase (GST). A mixed pattern of age-associated alterations in antioxidant activities was observed. SOD, GSH-Px and GST activities were increased with age, but CAT activity was decreased. Lung SOD, GSH-Px and GST activities were also increased in response to SO₂. The level of TBARS was increased with age. SO₂ exposure stimulated lipid peroxide formation in the lung as indicated by an increase in the level of TBARS. These findings suggest that both aging and SO₂ exposure may impose an oxidative stress to the body. We conclude that the increase in the activities of the antioxidant enzymes of the lung during aging, could be interpreted as a positive feedback mechanism in response to rising lipid peroxidation.     

Effects of X-ray radiation on lipid peroxidation and antioxidant systems in rabbits treated with antioxidant compounds

The aim of this study was to investigate the effects of supplemental antioxidant vitamins and minerals on lipid peroxidation and on the antioxidant systems in rabbits exposed to X-rays. The rabbits were divided into two experimental groups and one control group, each group containing seven rabbits. The first group (VG) received daily oral doses of vitamin E (460 mg/kg live weight) and vitamin C (100 mg/kg live weight). The second group (MG) was fed a mineral-enriched diet that contained 60 mg manganese chloride, 40 mg zinc sulfate, and 5 mg copper sulfate per kilogram of feed. The third group served as controls and received only a standard diet. Blood samples were obtained before and after the supplementation with vitamins or minerals, as well as before and after irradiation with a total dose of 550-rad X-rays. The blood samples were analyzed for their content of malondialdehyde (MDA), plasma vitamins C and E, retinol, reduced glutathione (GSH), and glutathione peroxidase activity (GPx). After irradiation, the control group showed increased levels of MDA and activity of GPx (p<0.05), whereas the levels of GSH, vitamin C, and vitamin E were decreased. In the VG, the concentration of MDA was lower (p<0.05), and the concentration of GSH and vitamins C and E were higher (p<0.05) when compared to controls. In the MG, the concentrations of MDA, GSH, vitamin C, and retinol were not affected by the mineral administration and radiation. The level of vitamin E in the MG increased with mineral administration (p<0.05), but decreased after irradiation (p<0.05). For the control group, the level of GSH was higher than in the two experimental groups. After irradiation, the VG animals had vitamin E and C levels that were higher than in MG and control groups (p<0.05). The activity of GPx was not affected by vitamin or mineral supplementation or by irradiation. We conclude that the supplementation with antioxidant vitamins and minerals may serve to reinforce the antioxidant systems, thus having a protective effect against cell damage by X-rays.     

Effect of oxalomalate on lipid metabolism and antioxidant defense system in rats

The metabolic functions of NADP(+)-specific isocitrate dehydrogenase (ID2), which may participate in the production of NADPH and biosynthesis of fatty acids, are not yet clearly understood. Accordingly, the current study investigated the effect of oxalomalate, known as a competitive inhibitor of ID2 in vitro, on lipid metabolism and the cellular defense system in vivo. Male Sprague Dawley rats (3 weeks old) were divided into two groups, fed a pelletized AIN-76 semisynthetic diet for 8 weeks, and injected intraperioneally with either saline or oxalomalate (25 mg/kg BW) dissolved in saline every 2 days. Oxalomalate did not lower the body weight and adipose tissue weight significantly; however, it significantly lower the plasma leptin concentration (p < 0.000), plasma and hepatic triglyceride levels (p < 0.01, p < 0.05), and adipocyte lipoprotein lipase activity (p < 0.01) compared to the control group. Meanwhile, hepatic antioxidant enzyme activities, except for superoxide dismutase activity (p < 0.01), glutathione content, and thiobarbituric acid reactive substances levels were not significantly different between the groups. Therefore, the current data suggests that oxalomalate produces a triglyceride-lowering activity and play a possible inhibitory role in fat accumulation. Furthermore, it was not found to affect the most antioxidative enzyme activities, glutathione content, and thiobarbituric acid reactive substances levels in rats fed normal diet.     

Effects of administration of Embelin and Curcumin on lipid peroxidation, hepatic glutathione antioxidant defense and hematopoietic system during N-nitrosodiethylamine/Phenobarbital-induced hepatocarcinogenesis in Wistar rats

The effects of administration of Embelin (EMB) and Curcumin (CUR) on lipid peroxidation, hepatic glutathione antioxidant defense and hematopoietic cells were examined during N-nitrosodiethylamine (DENA-200 mg kg⁻¹body wt, single I.P injection) initiated and Phenobarbital (PB-0.05% in drinking water orally for 13 weeks) promoted hepatocarcinogenesis in Wistar strain male albino rats. DENA/PB-induced hepatic damage was manifested by a significant drop in the hepatic glutathione antioxidant defense, increased lipid peroxidation and histological alterations like dysplasia, and atypical cells with abnormal chromatin pattern. Treatment with Curcumin (100 mg kg⁻¹body wt) and Embelin (50 mg kg⁻¹body wt) prevented the drop in hepatic glutathione antioxidant defense, decreased lipid peroxidation, minimized the histological alterations induced by DENA/PB, but showed toxic effects on the hematopoietic cells. Results indicate the beneficial effects of Embelin and Curcumin against oxidative tissue damage during chemically-induced hepatocarinogenesis in rats.     

Effect of depletion of glutathione by buthionine sulfoximine on lipid peroxidation in rats acutely treated with ethanol

• 1.1. The effect of depletion of glutathione (GSH) by dl-buthionine-S,R-sulfoximine (BSO) on lipid peroxidation in rats acutely treated with ethanol was investigated.
• 2.2. BSO pretreatment has not been found to potentiate an increase in liver, brain and erythrocyte lipid peroxide levels.

     

Chemically-induced glutathione depletion and lipid peroxidation

Malondialdehyde (MDA) formation in mouse liver homogenates was measured in the presence of various glutathione depletors (5 mmol/l). After a lag phase of 90 min, the MDA formation increased from 1.25 nmol/mg protein to 14.5 nmol/mg in the presence of diethyl maleate (DEM), to 10.5 with diethyl fumarate (DEF) and to 4 with cyclohexenon by 150 min. It remained at 1.25 nmol/mg with phorone and in the control. On the other hand, glutathione (GSH) dropped from 55 nmol/mg to 50 nmol/mg in the control to, < 1 with DEM, to 46 with DEF, to 3 with cyclohexenon and to 7 with phorone. The data show that the potency to deplete GSH is not related to MDA production in this system. DEM stimulated in vitro ethane evolution in a concentration-dependent manner and was strongly inhibited by SKF 525A. From type I binding spectra to microsomal pigments the following spectroscopic binding constants were determined: 2.5 mmol/l for phorone, 1.2 mmol/l for cyclohexenon, 0.5 mmol/l for DEM and 0.3 mmol/l for DEF. In isolated mouse liver microsomes NADPH-cytochrome P-450 reductase and NADH-cytochrome b₅ reductase activity were unaffected by the presence of DEM, whereas ethoxycoumarin dealkylation was inhibited. Following in vivo pretreatment, hepatic microsomal electron flow as determined in vitro was augmented in the presence of depleting as well as non-depleting agents, accompanied by a shift from O₂⁻ to H₂O₂ production. It is concluded that it is not the absence of GSH which causes lipid peroxidation after chemically-induced GSH depletion but rather the interaction of the chemicals with the microsomal monoxygenase system.     

Function of the antioxidant system in rats exposed to cadmium

Lipid peroxidation (LPO) and antioxidant system functioning in the blood, liver and small intestine mucosal cells of rats under cadmium chloride intake and administration of the liposomal form of the biologically active supplement (BAS FLP-MD) have been studied. It is shown that cadmium chloride administration (1 mg/kg, 14 days) leads to the activation of the oxidative processes in the cells and decrease of the antioxidant enzyme activities including mitochondrial enzymes. The revealed inhibition of the hepatic superoxide dismutase (SOD) activity considerably determined by the effect on mitochondrial Cu, Zn-SOD. The effect of one-shot and long-term cadmium intake on the conjugation system and decrease of the tissue glutathione level were shown. BAS FLP-MD intake normalizes the oxidative processes possibly due to stabilization of the cellular components.     

Effect of nickel chloride on hepatic lipid peroxidation and glutathione concentration in mice

Intraperitoneal administration of nickel chloride enhanced hepatic lipid peroxidation (HLP) in 6-wk-old and 8–12-wk-old male CBA-mice but not in 3-wk-old mice. nickel chloride administration depleted hepatic GSH in 8–12-wk-old mice but not in the younger age groups. After 300 μmol NiCl₂/kg mortality occurred among 8–12-wk-old mice but not among the younger mice. Stimulation of GSH synthesis by administration ofl-2-oxothiazolidine-4-carboxylate reduced nickel chloride induced mortality and HLP. Reduction of GSH synthesis by administration of buthionine sulfoximine (BSO) did not, however, enhance the toxicity of nickel chloride. This might be owing to chelation of the Ni(II)-ion by BSO. The results demonstrate age dependency and a protective effect of enhanced GSH synthesis in nickel chloride stimulated HLP.     

Effect of unithiol and acetylcysteine on lipid peroxidation and the erythrocyte antioxidant system in sensitized guinea pigs

The effect of unithiol and acetylcysteine on lipid peroxidation, thioldisulfide equilibrium, glucose-6-phosphate dehydrogenase, glutathione reductase and lactate dehydrogenase activity and on erythrocyte resistance was studied in guinea-pigs during sensitization with C. maltosa. Sensibilized animals receiving thiol antioxidants showed partial restoration of normal biochemical levels.     

Aqueous date fruit extract protects against lipid peroxidation and improves antioxidant status in the liver of rats subchronically exposed to trichloroacetic acid

Trichloroacetic acid (TCA) is a prominent by-product of the chlorination of drinking water. It induces cell damage by producing free radicals and reactive oxygen species. The present study was carried out to evaluate the potential hepatoprotective role of the aqueous date extract (ADE) against TCA-induced liver injury. Forty-eight male Wistar rats were randomly divided into six groups of eight: group I served as the control; group II was given ADE by gavage; groups III and IV received TCA as drinking water at 0.5 and 2 g/L, respectively; and groups V and VI were treated with ADE by gavage and then received TCA at 0.5 and 2 g/L, respectively, as drinking water. The experiment was performed for 2 months. The hepatotoxicity of TCA administration was revealed by an increase in the levels of hepatic marker enzymes (transaminases, gamma-glutamyl transferase, and lactate dehydrogenase) and conjugated bilirubin and a decrease in albumin level. The TCA administration induced also significant elevation of the malondialdehyde (MDA) level and the antioxidant activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx) paralleled with a significant decline in catalase (CAT) activity. These biochemical alterations were accompanied by histological changes marked by the appearance of vacuolization, necrosis, congestion, inflammation, and enlargement of sinusoids in the liver section. Treatment with date palm fruit extract restored the liver damage induced by TCA, as demonstrated by inhibition of hepatic lipid peroxidation; amelioration of SOD, GPx, and CAT activities; and improvement of histopathology changes. These results suggest that ADE has a protective effect over TCA-induced oxidative damage in rat liver.     

Aging and lung antioxidant enzymes, glutathione, and lipid peroxidation in the rat.

The five major antioxidants enzymes, cytochrome oxidase (COX), GSH, and GSSG, and endogenous and in vitro stimulated lipid peroxidation (TBA-RS) were assayed in the lung of old (28 months) and young (9 months) adult rats due to the almost total absence of data of this kind in this tissue, which is normally exposed to relatively high pO2 throughout life. Catalase, selenium (Se)-dependent GSH peroxidase (GPx), GSH reductase, GSH, GSSG, GSSG/GSH, and in vivo and in vitro TBA-RS showed similar values in old and young animals. The decrease observed for non Se-dependent GPx disappeared when the values were expressed in relation to COX activity. Only superoxide dismutase showed a clear decrease when referred both to protein and COX activity. These results suggest that lung aging is not accelerated in old age due to a decrease in the antioxidant capacity of the tissue. Nevertheless, they are compatible with a continuous damage of the lung tissue by free radicals throughout the life span.