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1.
In this communication, we show the modulatory potential of papaverine, an opium alkaloid and a well known vasodilator agent on the ethanol-induced hepatic oxidative stress in male Wistar rats. Ethanol treatment (50% v/v) enhanced lipid peroxidation significantly accompanied by a decline in the activities of glutathione peroxidase (G-Px), glutathione reductase (GR) and depletion in levels of hepatic glutathione (GSH). Ethanol administration increased hepatic glutathione-s-transferases (GST). Enhanced lipid peroxidation induced by ethanol was significantly reduced when papverine was coadministered (P<0.05). In addition, the depleted levels of glutathione and inhibited activities of G-Px and GR recovered significantly (P<0.05) levelling off to control values on co-exposure. Papaverine (200 mg/kg bw) effectively antagonised the ethanol-induced lipid peroxidation and impaired glutathione levels and glutathione dependent enzyme systems. Our results suggest that papaverine is an effective chemopreventive agent in the liver and may suppress the ethanol-induced hepatotoxicity.  相似文献   

2.
BackgroundAscorbic acid (Asc) is one of the most abundant antioxidants and it serves as a major contributor to protect plants against oxidative damage. Plants use two enzymes that participate in the metabolic recycling of Asc. One of these two enzymes is dehydroascorbate reductase (DHAR). It directly regenerates Asc from its oxidized state and thus prevents Asc from being irreversibly hydrolyzed to 2, 3-diketogulonic acid. This study aimed to examine whether over-expression of DHAR leads to an enhanced oxidative stress tolerance in tobacco plants.ResultsIn this study, we functionally characterized a novel JcDHAR gene from Jatropha curcas and found via quantitative RT-PCR analysis that JcDHAR can be induced with H2O2, salt and PEG stresses. The DHAR activities of transgenic tobacco plants increased from 2.0 to 5.3 fold compared to wild-type plants. As a result, the transgenic plants displayed enhanced tolerance to oxidative stress.ConclusionsOur results indicate that JcDHAR expression can effectively enhance the tolerance to oxidative stress in plants.  相似文献   

3.
The study was undertaken to evaluate the possible involvement of oxidative stress in the pathogenesis of ethanol induced testicular atrophy in rats. Adult male rats were orally administered ethanol at a dose of 1.6 g/kg body weight/day for four weeks. Twenty-four hours after the last treatment the rats were sacrificed using anesthetic ether. Testes were removed and weighed. Apoptosis was studied by using the Feulgen reaction on 5 μ thin paraffin sections of testis. Testicular homogenate was prepared and centrifuged. The supernatant was used for the estimation of extent of lipid peroxidation and antioxidant defense status. There was significant reduction in body weight: and in testicular weight and diameter in ethanol treated rats. Extent of germ cell apoptosis was significantly high in ethanol treated rats. Ethanol treated rats showed significantly high tissue TBARS level and glutathione S-transferase activity; and low tissue ascorbic acid, reduced glutathione, superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase activities. Chronic ethanol administration resulted in high oxidative stress in the testes either due to increased extent of lipid peroxidation or due to decreased antioxidant defenses, and thereby induces germ cell apoptosis leading to testicular atrophy.  相似文献   

4.
Damaging effects of reactive oxygen species on living systems are well documented. They include oxidative attack on vital cell constituents. Chronic ethanol administration is able to induce an oxidative stress in the central nervous system. In the present study, 16–18 week-old male albino rats of Wistar strain were exposed to different concentration of ethanol for 4 weeks. This exposure showed profound effect on body weight. Ascorbic acid level; and activities of alkaline phosphatase and aspartate transaminase in the brain are dependent on the concentration of ethanol exposure. Chronic ethanol ingestion elicits statistically significant increase in thiobarbituric acid reactive substances level and decrease in gluatathione level in the brain. It reduces superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase activities in a dose dependent manner. However, histological examination could not reveal any pathophysiological changes. Therefore, we conclude that biochemical alterations and oxidative stress related parameters respond early in alcoholism than the histopathological changes in brain.  相似文献   

5.
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6.
Ethanol-induced liver injury may be linked, at least partly, to an oxidative stress resulting from increased free radical production and/or decreased antioxidant defence. Distinguishing alcoholic and non-alcoholic liver disease has important implications. This study looked at the possible changes between alcoholic and non-alcoholic liver diseases by examining the presence of oxidative damage, as monitored by several parameters relating to oxidative stress. Lipid peroxides concentration, superoxide dismutase activity and glutathione S-transferase activity increased, where as glutathione content, glutathione peroxidase activity and glutathione reductase activity decreased among the tested subjects in comparison to normal healthy group. Determination of these parameters may be valuable in the evaluation of liver disease. However, oxidative stress related enzymes and non-enzymes can not be utilized as a marker for alcoholic liver diseases, as these parameters responded in the same way after liver is damaged irrespective of their cause. Their level may help in determining the degree of liver damage. Degree of oxidative injury was similar in patients with non-alcoholic liver disease and in moderate drinkers; while significantly higher in heavy drinkers. The differences between the groups might be based on the type of liver pathological condition rather than its etiology (i.e. alcohol and non alcohol related causes).  相似文献   

7.
Thiamine or vitamin B1 is a well known coenzyme and nutrient necessary for the assembly and right functioning of several enzymes involved in the energy metabolism. The present study evaluates oxidative stress and prevalence of neurodegenerative conditions in the brain following TD. The study was carried out on mice (Musmusculus) in three groups, namely control and thiamine-deficient group for 8 (TD 8) and 10 (TD 10) days. Lipid peroxidation was determined in terms of reduced glutathione (GSH) and thiobarbituric acid reactive substance (TBARS). The level of antioxidant enzymes such as catalase (CAT), glutathione reductase, glutathione peroxidase (GPx), superoxide dismutase (SOD) and glutathione transferase (GST) were measured along with histopathological studies in all the groups. There was significant increase in the TBARS levels in group II (TD 8) and group III (TD 10) animals in comparison to controls (Group I). The GSH levels were found to be lower in both the treated groups. The level of antioxidant enzymes CAT (p < 0.001), glutathione reductase (p < 0.001), GPx (p < 0.001), SOD (p < 0.0001) were found to be significantly reduced in group III (TD 10) in comparison to controls. Histopathological studies showed moderated to extensive neuronal loss in group II and group III in comparison to control group. The increase in LPO and reduction in enzymes CAT, glutathione reductase, GPx, SOD, and GST following TD suggests mitochondrial dysfunction, neuronal loss acute oxidative stress that may impair the functioning of the brain along with the rise of neurodegenerative conditions in the affected animals.  相似文献   

8.
Alcohol induced oxidative stress is linked to the metabolism of ethanol. In this study it has been observed that administration of ethanol in lower concentration caused gain in body and liver weight. while higher concentration of ethanol caused lesser gain in body and liver weight. Ethanol treatment enhanced lipid peroxidation significantly, depletion in levels of hepatic glutathione and ascorbate, accompanied by a decline in the activities of glutathione peroxidase and glutathione reductase, and increased in hepatic glutathione s-transferase activity. Interestingly catalase activity increases in lower concentration of ethanol exposure, and decreased in higher concentration. Superoxide dismutase activity was also increased on ethanol exposure. But, ethanol feeding did not show any effect on glucose-6-phosphate dehydrogenase activity. Ethanol ingestion perturbs the antioxidant system in a dose and time dependent manner.  相似文献   

9.
After administration, ethanol and its metabolites go through the kidneys and are excreted into urine. The kidney seems to be the only vital organ generally spared in chronic alcoholics. Therefore, we investigated the multiple effects of chronic ethanol exposure on renal function tests and on oxidative stress related parameters in the kidney. Chronic ethanol (1.6 g ethanol/ kg body weight/ day) exposure did not show any significant change in relative weight (g/ 100g body weight) of kidneys, serum calcium level or glutathione s-transferase activity. However, urea and creatinine concentration in serum, and TBARS level in kidney elevated significantly, while reduced glutathione content and activities of glutathione peroxidase, glutathione reductase and superoxide dismutase diminished significantly after 12 weeks of ethanol exposure. Catalase activity showed increased activity after 4 weeks of ethanol exposure and decreased activity after 12 weeks of ethanol exposure. Genesis of renal ultrastructural abnormalities after 12 weeks of ethanol exposure may be important for the development of functional disturbances. This study revealed that chronic ethanol exposure for longer duration is associated with deleterious effects in the kidney.  相似文献   

10.
Preeclampsia is a multisystem disorder involves altered homeostasis of oxidants–antioxidants, inflammatory process and endothelial dysfunction. The present study aim was to determine the levels of oxidative stress parameters (malondialdehyde, protein carbonyl, ischemia modified albumin and xanthine oxidase), nutrient antioxidants (vitamin C and vitamin E), enzyme antioxidants (catalase, superoxide dismutase, glutathione peroxidase glutathione reductase), total antioxidant status (TAS) and its association with nitric oxide. The study population consists of three groups, non pregnants (Group 1, n = 57), normotensive pregnants (Group 2, n = 57) and Preeclampsia (Group 3, n = 57). Group 2 and 3 were followed after delivery within 48 h. In preeclampsia xanthine oxidase, malondialdehyde and uric acid levels were significantly increased (p < 0.001), while TAS decreased (p < 0.05) when compared to normotensive pregnant and non pregnant. Catalase, glutathione reductase levels were increased (p < 0.005) and vitamin E, super oxide dismutase levels were decreased (p < 0.001) in preeclampsia when compared to normal pregnants. Receiver operating characteristics curve analysis showed area under curve for xanthine oxidase (0.8), malondialdehyde (0.804), Uric acid (0.84), ischemia modified albumin (0.92) and catalase (0.88) which indicated as good markers in preeclampsia. Amongst, ischemia modified albumin is a better marker of intrauterine hypoxic reperfusion risk with sensitivity 87.7 % and specificity 91.2 %. The increased hydrogen peroxide from xanthine oxidase adds to oxidative stress and increased catalase activity in preeclampsia represents combating action. Increased oxidative stress, decreased TAS and its apparent reversible changes evinced within 48 h after delivery in preeclampsia illustrated that placental abnormality is the contributing factor in the pathogenesis.  相似文献   

11.
To study the mechanism of action of water soluble compound GII purified from fenugreek (Trigonella foenum graecum) seeds which was shown earlier to have antidiabetic effect in the subdiabetic, moderately and severely diabetic rabbits. In rabbits (1–1.5 kg bw) diabetes was induced by intravenous injection of 80 mg/kg bw of alloxan. They were fed with GII at a dose of 50 mg/kg bw daily once in the morning for 15 days in the subdiabetic and moderately diabetic and 30 days in the severely diabetic rabbits. Serum total cholesterol (TC), triglycerides (TG), LDL + VLDL cholesterol [(LDL + VLDL)C], HDL cholesterol [(HDL)C], total tissue lipids, glycogen and enzymes of carbohydrate metabolism (glycolysis, gluconeogenesis, polyol pathway) hexokinase, glucokinase, pyruvate kinase, malic enzyme, glucose-6-phosphatase, glucose-6-phosphate dehydrogenase, aldose reductase and sorbitol dehydrogenase and antioxidant enzymes glutathione peroxidase, glutathione reductase and superoxide dismutase were estimated. Liver and kidney function parameters were also estimated. Treatment with GII for 15 days in the subdiabetic and moderately diabetic rabbits and for 30 days in the severely diabetic rabbits (i) decreased the elevated lipids TC, TG, (LDL + VLDL)C and increased the decreased (HDL)C, (ii) decreased the elevated liver and heart total lipids, TC and TG, (iii) increased the decreased liver and muscle glycogen, (iv) increased the decreased hexokinase, glucokinase, pyruvate kinase, malic enzyme, glucose-6-phosphate dehydrogenase, superoxide dismutase, glutathione peroxidase, (v) decreased the increased glucose-6-phosphatase, sorbitol dehydrogenase, aldose reductase. Results thus show that treatment with GII compound purified from fenugreek seeds for 15 days in the subdiabetic and moderately diabetic and 30 days in the severely diabetic rabbits corrects the altered serum lipids, tissue lipids, glycogen, enzymes of glycolysis, gluconeogenesis, glycogen metabolism, polyol pathway and antioxidant enzymes. Histopathological abnormalities (fatty infiltration and other cellular changes) seen in the pancreas, liver, heart and kidneys were repaired after treatment with GII. In fact partially damaged pancreas was repaired. Liver and kidney function test results were normal in the GII treated animals indicating that GII treatment is safe and free from any side effects.  相似文献   

12.
Aflatoxins are potent hepatotoxic and hepatocarcinogenic agents. Reactive oxygen species and consequent peroxidative damage caused by aflatoxin are considered to be the main mechanisms leading to hepatotoxicity. The present investigation aims at assessing the hepatoprotective effect of ethanolic leaves extract of Trianthema portulacastrum on aflatoxin B1 (AFB1)-induced hepatotoxicity in a rat model. The hepatoprotection of T. portulacastrum is compared with silymarin, a well known standard hepatoprotectant. Lactate dehydrogenase, alkaline phosphatase, alanine and aspartate aminotransferases were found to be significantly increased in the serum and decreased in the liver of AFB1 administered (1 mg/kg bw, orally) rats, suggesting hepatic damage. Marked increase in the lipid peroxide levels and a concomitant decrease in the enzymic (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase and glutathione-S-transferase) and nonenzymic (reduced glutathione, vitamin C and vitamin E) antioxidants in the hepatic tissue were observed in AFB1 administered rats. Pretreatment with T. portulacastrum (100 mg/kg/p.o) and silymarin (100 mg/kg /p.o) for 7 days reverted the condition to near normal. The results of this study indicate that the ethanolic leaves extract of T. portulacastrum is a potent hepatoprotectant as silymarin.  相似文献   

13.
Alcohol consumption and health outcomes are complex and multidimensional. Ethanol (1.6g / kg body weight/ day) exposure initially affects liver function followed by renal function of 16–18 week-old male albino rats of Wistar strain weighing 200–220 g. Chronic ethanol ingestion increased in thiobarbituric acid reactive substances level and glutathione s-transferase activity; while decreased reduced gluatathione content and activities of catalase, glutathione peroxidase and glutathione reductase in a time dependent manner in the hemolysate. Though superoxide dismutase activity increased initially might be due to adaptive response, but decreased later. Elevation of serum nitrite level and transforming growth factor-b1 activity indicated that long-term ethanol consumption may cause hepatic fibrosis and can elicit pro-angiogenic factors. However, no alteration in vascular endothelial growth factor-C activity indicated that ethanol consumption is not associated with lymphangiogenesis. Therefore, we conclude that long-term ethanol-induced toxicity is linked to an oxidative stress, which may aggravate to fibrosis and elevate pro-angiogenic factors, but not associated with lymphangiogenesis.  相似文献   

14.
A disturbance in the antioxidant defense system including α-tocopherol, ascorbic acid and reduced glutahtione metabolism due to free radical induced oxidative injury has been implicated in various neuro-psychiatric disorders. The roles of these antioxidants, changes in their blood levels and correlation with oxidative stress were studied in a common psychiatric illness Schizophrenia. Fifty-eight subjects of either sex ranging in age from 18–60 years divided into two age groups (≤40 and >40 years) diagnosed for schizophrenia, and forty age and sex-matched normal subjects as controls were included in the study. Blood samples were analyzed for malondialdehyde (MDA), α-tocopherol, total ascorbic acid (TAA), dehydro ascorbic acid (DHAA), reduced ascorbic acid (RAA), leucocyte ascorbic acid (LAA) and reduced glutathione (GSH). A decrease in the levels of α-tocopherol, total ascorbic acid and reduced glutathione was found in schizophrenics compared to normal controls. Further a significant rise in oxidative stress and decreased antioxidant status was observed in the chronic stage of schizophrenia as compared to those in acute condition. A significant rise in dehydroascorbic acid with concomitant fall in reduced ascorbic acid suggests scavenging action of ascorbic acid and its utilization with increased oxidative stress as indicated by high blood malondialdehyde levels. Leucocyte ascorbic acid, a better index of ascorbic acid status was also found to be reduced in schizophrenics, suggesting depletion of body stores of ascorbic acid and the condition worsened with advancing age.  相似文献   

15.
The changes in the erythrocyte lipid peroxidation products (MDA), levels of glutathione (GSH), ascorbic acid and plasma vitamin E (non enzymatic antioxidant parameters) and activities of antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase in erythrocytes and plasma glutathione - S - transferase (GST) activity were estimated in patients with rheumatoid arthritis. This work was undertaken to assess oxidative stress and anti oxidant status in patients with rheumatoid arthritis. It was observed that there was a significant increase in erythrocyte MDA levels, activities of SOD, GPX, plasma GST and a significant decrease in erythrocyte GSH, ascorbic acid, plasma vitamin E levels and catalse activity in patients with rheumatoid arthritis when compared to controls. The results of our study suggests higher oxygen free radical production, evidenced by increased MDA and decreased GSH, ascorbic acid, vitamin E and Catalase activity, support to the oxidative stress in rheumatoid arthritis. The increased activities of antioxidant enzymes may be a compensatory regulation in response to increased oxidative stress.  相似文献   

16.
Glucose-6-phosphate dehydrogenase (G6PD), a cytoplasmic enzyme, plays a protective role during oxidative stress in eucaryotic cells, since they provide coenzymes and substrates to the primary antioxidant enzymes. The redistribution of G6PD in the hippocampus was studied post-ischemia (PI). There was a characteristic localisation of G6PD in pyramidal cell layers of the rat hippocampus. In hippocampus CA1 cells were stained weakly whereas CA3 cells showed strong histochemical staining. Ischemia induced up-regulation of G6PD in the hippocampus was in a specific manner. First, the activity increased in the whole hippocampus (at 4 hours PI) which persisted 6 hrs PI in CA1 area. However G6PD activity decreased in the CA3 area & dentate gyrus. At 10 & 24 hrs PI, activity decreased in CA1 area but normalised in CA3 area & dentate gyrus compared to controls. This suggests that the sensitive CA1 neurons are transiently capable of generating an anti-oxidative arsenal to cope with the oxidative stress in the first few hours PI. We can conclude that the brain contains inducible endogenous mechanisms that are capable of enhancing the ability of neurons to withstand lethal ischemic challenge. (Presently working in Vardhman Mahavir Medical College & Safdarjung Hospital, New Delhi)  相似文献   

17.
Oxidative stress is implicated in the etiopathogenesis of a variety of human diseases. Therefore, in the present study, erythrocyte lipid peroxidation, percentage hemolysis, antioxidant enzymes viz., glutathione reductase, glutathione peroxidase, superoxide dismutase and plasma antioxidants viz., ceruloplasmin, vitamins A,E and C have been determined in 19 patients with tubercular meningitis (TBM) and 50 normals. Six patients who were treated with antibiotics were considered for the follow up. The statistical analysis was carried out by Mann Whitney U test and Wilcoxon rank sum test. Lipid peroxidation (P<0.02), percentage hemolysis (P<0.001) and plasma ceruloplasmin (P<0.0001) of TBM patients were significantly higher, whereas erythrocyte glutathione reductase (P<0.05) and plasma antioxidant vitamins A, E and C (P<0.01, P<0.05 respectively) were significantly lower than those of the controls. In the follow up patients the glutathione reductase and catalase levels were significantly high (P<0.05) compared to their pre-treated condition. Vitamin C and E levels have attained normal range. This study indicated that the blood antioxidant status of TBM patients which was low compared to controls improved after treatment, suggesting the role of free radicals in TBM.  相似文献   

18.
In this study antioxidant activity of methanol extract of rhizomes ofCurculigo orchioides (MEC) was investigated using carbon tetrachloride (CCl4)-intoxicated rat liver as the experimental model. The hepatotoxic rats were administered MEC for 90 days (daily, orally at the dose of 70 mg per kg body weight). Lipid peroxidation (LPO) in CCl4-intoxicated rats was evidenced by a marked increment in the levels of thiobarbituric acid reactive substances (TBARS) and diene conjugates (CD), and also a distinct diminution in glutathione (GSH) content in the liver. In CCl4+MEC—treated rats these biochemical parameters attained an almost normal level. The decreased activity of antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and glutathione reductase (GRD) in CCl4—intoxicated rats, and its retrieval towards near normalcy in CCl4+MEC—administered rats revealed the efficacy of MEC in combating oxidative stress due to hepatic damage. Elevated level of glutathione transferase(GTS) observed in hepatotoxic rats too showed signs of retuming towards normalcy in MEC co-administered animals, thus corroborating the antioxidant efficacy of MEC. The findings provide a rationale for further studies on isolation of active principles and its pharmacological evaluation.  相似文献   

19.
Reactive oxygen species (ROS) cause damage to the DNA producing mutations and formation of tumours such as carcinoma of breast. Tumour cells are known to produce ROS at a greater pace than the non-transformed cells. The increased production of reactive oxygen species causes oxidative stress leading to cell proliferation and hence increased inflammatory conditions. The present study was aimed to investigate the role of oxidative stress in the pathogenesis of breast cancer. Females suffering from breast cancer had significantly decreased Superoxide dismutase (SOD) and reduced glutathione (GSH) levels in comparison to normal females. The compromised antioxidant defence system produces the oxidative stress which in turn creates the inflammatory response shown by concomitant increased adenosine deaminase (ADA) activity in female patients. ADA diminishes the protective molecule adenosine. There were significant variations (p < 0.01) in ADA activity with different clinical stages (stage 1–4) of breast cancer suggesting thereby that estimation of ADA activity can be used as a diagnostic tool to detect the stage of cancer along with cytological studies. Mastectomy was performed and post-operatively serum SOD and ADA activity and plasma GSH levels were estimated. There was a statistically significant increase in activity of SOD and levels of GSH while serum ADA activity decreased significantly, suggesting thereby that oxidative stress is responsible for increased cell proliferation and hence the inflammatory conditions in CA breast that got ameliorated post-operatively.  相似文献   

20.
Radiation induced brain damage is associated with impairment of mitochondrial functions, variations in the level of neurotransmitters, and oxidative stress. Mitochondrial function is closely linked to the level of neurotransmitters since the precursors are supplied by the Kreb’s cycle intermediates. The objective of this study was to evaluate the influence of pantothenic acid, an essential component in the synthesis of Coenzyme A (CoA), on the activity of the Krebs cycle enzymes, isocitrate dehydrogenase (IDH), α-ketoglutarate dehydrogenase (α-KGDH), and succinate dehydrogenase (SDH); the level of aspartic, glutamic and GABA; the activity of transaminases, and oxidative stress, in the cerebrum of γ-irradiated rats. Pantothenic acid (26 mg/Kg) was orally administered to the rats, 2 h after irradiation and during the following 5 days. Animals were sacrificed the 7th day post-irradiation. The exposure of male albino rats to γ-rays (5 Gy) has triggered oxidative stress notified by a significant elevation in the level of malondialdehyde (MDA), an end product of lipid peroxidation, associated to a significant decrease in the content of phospholipids, and the antioxidant compound glutathione (GSH). The activity of IDH, α-KGDH, and SDH, has significantly decreased, while the level of aspartic, glutamic and GABA has significantly increased. In parallel to these changes, the activity of alanine and aspartate transaminase has significantly increased, compared to their values in the control rats. Pantothenic acid treatment, has significantly attenuated oxidative stress; enhanced the activity of IDH, α-KGDH, and SDH; minimized the increase in the level of amino acids and the activity of transaminases, compared to their values in the cerebrum of irradiated rats. In conclusion, pantothenic acid could improve the level of neurotransmitters amino acids, which depends on the enzymatic activities of Krebs cycle and linked to oxidative stress.  相似文献   

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