Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1260386 (GSH)
 38,102 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We examined the role of selenium (Se) in the mechanism of oxidative stress caused by endotoxin by feeding rats deficient a diet in this element. In rats fed the Se-deficient diet (concentration of Se, less than 0.027 microg g(-1)) for 10 weeks, Se level and glutathione peroxidase (GSH-Px) activity in the liver were about 47 and 43% lower, respectively, than those in rats fed a Se-adequate diet (Se, 0.2 microg g(-1)). Rat fed the Se-deficient diet and given endotoxin (6 mg kg(-1), i.p.) showed a mortality rates of about 43% at 18 h. Nevertheless, no lethality was observed with endotoxin (4 mg kg(-1), i.p.) challenge. Levels of serum lactate dehydrogenase and acid phosphatase leakage were significantly higher in Se-deficient rats than those in Se-adequate diet 18 h after endotoxin (4 mg kg(-1), i. p.) challenge. Superoxide anion generation and lipid peroxide formation in the liver of Se-deficient rat were markedly increased 18 h after endotoxin (4 mg kg(-1), i.p.) injection compared with those in the endotoxin/Se-adequate diet group, whereas non-protein sulfhydryl level in the liver after administration of endotoxin to Se-deficient rats was lower than that in Se-adequate rats treated with endotoxin. We investigated whether Se can suppress nitric oxide (NO) generation and cytotoxicity in endotoxin-treated J774A.1 cells. Treatment with Se (10(-6) M) markedly inhibited endotoxin (0.1 microg ml(-1))-induced NO production in J774A.1 cells. Se induced an increased activity of GSH-Px in cells after 24 h of incubation, suggesting that the preventive effect of Se on NO production in endotoxemia is due to the induction of Se-GSH-Px activity. However, Se did not affect endotoxin-induced cytotoxicity in J774A.1 cells. These findings suggested that the oxidative stress caused by endotoxin may be due, at least in part, to changes in Se regulation during endotoxemia.
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PMID:Roles of selenium in endotoxin-induced lipid peroxidation in the rats liver and in nitric oxide production in J774A.1 cells. 1113 11

S-(1-Acetoxymethyl)glutathione (GSCH(2)OAc) was synthesized and used as a model for the reaction of glutathione (GSH)-dihaloalkane conjugates with nucleosides and DNA. Previously, S-[1-(N(2)-deoxyguanosinyl)methyl]GSH had been identified as the major adduct formed in the reaction of GSCH(2)OAc with deoxyguanosine. GSCH(2)OAc was incubated with the three remaining deoxyribonucleosides to identify other possible adducts. Adducts to all three nucleosides were found using electrospray ionization mass spectrometry (ESI MS). The adduct of GSCH(2)OAc and deoxyadenosine was formed in yield of up to 0.05% and was identified as S-[1-(N(7)-deoxyadenosinyl)methyl]GSH. The pyrimidine deoxyribonucleoside adducts were formed more efficiently, resulting in yields of 1 and 2% for the GSCH(2)OAc adducts derived from thymidine and deoxycytidine, respectively, but their lability prevented their structural identification by (1)H NMR. On the basis of the available UV spectra, we propose the structures S-[1-(N(3)-thymidinyl)methyl]GSH and S-[1-(N(4)-deoxycytidinyl)methyl]GSH. Because adduct degradation occurred most rapidly at alkaline and neutral pH values, an enzymatic DNA digestion procedure was developed for the rapid hydrolysis of DNA to deoxyribonucleosides at acidic pH. DNA digests were completed in less than 2 h with a two-step method, which consisted of a 15 min incubation of DNA with high concentrations of deoxyribonuclease II and phosphodiesterase II at pH 4.5, followed by incubation of resulting nucleotides with acid phosphatase. Analysis of the hydrolysis products by HPLC-ESI-MS indicated the presence of the thymidine adduct.
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PMID:Characterization of nucleoside and DNA adducts formed by S-(1-acetoxymethyl)glutathione and implications for dihalomethane-glutathione conjugates. 1136 61

Xanthoparmellia mexicana was successfully isolating and culturing from its two symbionts and, preliminarily re-symbiosising its thalli in vitro performed from pure cultured photobiont and mycobiont. The solution exposure method was applied, confirming the toxic effect of sulfite solution with pH 4.0. The biochemical responses of lichen thalli and cultured symbionts to the short time stress of SO2 were studied. The chlorophyll PQa value of photobiont was correlated with its absorption of SO2. Chlorophyll a was more sensitive than chlorophyll b; chlorophyll was damaged most severely by the exposure of 0.5 mg.L-1 of SO2 fumigation, but was aggravated with the increase in the concentration of SO2 by way of solution exposure. The activity of acid phosphatase in lichen was mainly dependent on the photobiont. Reduced glutathione(GSH) was activated by oxidative stress of SO2. GSH was confirmed to be highly correlated with SO2 stress, and was proposed to be a significant and prospective biomarker of the status of lichen antioxidant system and the oxidative damage in lichen. The mycobiont was proposed to mainly resist the oxidative stress by SO2, while the photobiont was damaged more easily with energy depletion.
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PMID:[Effects of sulphur dioxide on the relationship between symbionts in lichen]. 1199 15

The Al-tolerant cultivar TAM202 and the Al-sensitive cultivar TAM 105 of winter wheat (Triticum aestivum L.) were exposed to 0, 50, 75, 100 or 150 microM of Al. The absorption of Al by wheat, the growth of root, several key enzymes concerned with C, N and P metabolism, as well as key constituents of antioxidant system, were investigated. The results showed that TAM105 absorbed more Al than TAM202 and its root growth (presented by the length) was inhibited more severely. The root growth was most closely related to mononuclear Al (Ala) activity. The metabolic enzymes (presented by glucose-6-phosphate dehydrogenase, nitrate reductase and acid phosphatase) in TAM202 were Al-tolerant. Presented by superoxide dimutase (SOD) and the content of reduced glutathione (GSH) and malondialdehyde (MDA), antioxidant system in TAM202 indicated lower oxidative stress and greater ability to protect the cultivar.
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PMID:Effects of aluminum on physiological metabolism and antioxidant system of wheat (Triticum aestivum L.). 1199 40

The dust generated during weaving (carpet dust) tibbati, knotted and tuffted carpets in carpet industry was studied for its toxicity in vitro and in vivo. Carpet dust (0.5, 1.0, 2.5 and 5.0 mg/1 x 10(6) cells) caused in vitro cytotoxicity in rat alveolar macrophages (AM) in a concentration-dependent manner. The cytotoxic, inflammatory and oxidative responses were observed in bronchoalveolar lavage fluid (BALF) of rats at 1, 4, 8 and 16 days after exposure. Rats were intratracheally exposed at 5 mg/rat individually to all three types of carpet dust. All types of carpet dusts produced increased AM, lymphocytes (PMN) population in BALF suggesting their inflammatory reactions. Cytotoxic nature of carpet dust was shown by the increased activities of lactate dehydrogenase (LDH) and acid phosphatase (AP) in BALF. Increased AM population and in vitro cytotoxicity due to carpet dusts have shown some correlation with the levels of LDH and AP activities in BALF. The gradual enhanced profile of hydrogen peroxide (H2O2) and nitric oxide (NO) along with depletion of reduced glutathione (GSH) in AM due to these carpet dusts are suggestive of their oxidant nature. The enzyme activities of both glutathione peroxidase (GPx) and glutathione reductase (GR) in AM were marginally reduced in exposed rats. In conclusion, the data suggest the cytotoxic, inflammatory and oxidant nature of carpet dusts. It is extrapolated that health effects on carpet weavers would be associated with the concentration and nature of airborne dust generated during weaving of carpets.
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PMID:Pulmonary toxicity of dust generated during weaving of carpets. 1254 37

The efficacy of two monothiols, N-acetyl-DL-homocysteine thiolactone (NAHT) and glutathione (GSH) either alone or in combination with two vitamins, vitamin B complex and vitamin E were studied in 7 days methylmercury chloride (MMC; I mg kg) intoxicated male Swiss albino mice. Thirteen groups of animals, each containing 6 animals were used for the study. Three groups of animals were kept as control (treated either with vehicle, normal saline or olive oil). Rest of the ten groups were kept as treatment groups. All the animals were treated subcutaneously for 7 days with MMC and one group was sacrificed on the 8th day. The second group was kept without toxicant for another 7 days and were sacrificed on the 15th day. Two MMC pretoxicated groups were treated either with vitamin B complex (20 mg kg) or vitamin E (60 mg kg) and two other groups were treated with N-acetyl-DL-homocysteine thiolactone (40 mg kg) or glutathione (50 mg kg) for another 7 days. The rest of the four groups were treated with either N-acetyl-DL-homocysteine thiolactone or glutathione in combination with either vitamin B complex or vitamin E. All the animals were sacrificed on the 15th day, brain and spinal cord were dissected and estimated for acid phosphatase, alkaline phosphatase, succinic dehydrogenase and alpha mannosidases. Some of the antidotes showed significant recovery of the enzymes in one tissue while some showed significant recovery in the other tissue depicting the need for treating methylmercury poisoned animals with multi-chelation therapy rather than as a monotherapy.
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PMID:Organelle specific enzyme markers as indicators of methylmercury neurotoxicity and antidotal efficacy in mice. 1257 86

Acute and sub-acute toxic effects of a novel phosphorothionate coded as RPR-II on testis of albino rats were studied. In acute study rats received a single dose of 12.3 mg/kg of RPR-II and sacrificed after 24 hr. For sub-acute study 0.58 mg/kg/day was administered orally to rats for 10 and 21 days. Acute exposure of rats to RPR-II brought no change either in the gonadosomatic index (GSI) or in the structure of testis or in the serum levels of testosterone. Testis glutathione (GSH) level and glutathione S-transferase (GST) activity was significantly decreased whereas, acid phosphatase (AcP) levels increased significantly at 24 hr post-treatment. On 7th day (withdrawal period) after the cessation of the treatment the GSH, GST, AcP, and AkP levels reached to near control. The sub-acute study revealed a significant decrease in GSI on 10th and 21st day of the treatment. In contrast, a time-dependent and significant increased in GSH level and GST activity was observed on 100th and 21st day of post-treatment, except GSH level on 10th day, which was declined. Due to RPR-II treatment the testis AcP and alkaline phosphatase (AkP) levels were significant at both 10th and 21st day of medication but AcP levels were increased whereas AkP levels decreased. The histopathological studies on day 10th showed considerable loss of spermatozoids in testis and at 21st day complete derangement of cellular organization was observed. Testosterone levels decreased significantly on 10th day and remained significantly low at 21st day. However, withdrawal studies showed a recovery in testis of rat treated with RPR-II. GST, GSH, GSI, AcP and AkP values recovered, testosterone levels were also well recovered but recovery in testis structure remained at a low profile. The present study suggests that RPR-II may cause testicular toxicity in rats affecting the normal functioning of testis and it also gave some new information in withdrawal studies.
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PMID:Acute and sub-acute effects of 2-butenoic acid-3-(diethoxy phosphinothioyl) methyl ester (RPR-II) on testis of albino rat. 1262 78

The present study was conducted to evaluate the therapeutic effectiveness of chelating agents [glutathione, 2,3 dimercapto propane sulfonic acid (DMPS) and D-penicillamine (DPA)] in combination with antioxidant (sodium selenite) in beryllium induced toxicity in female rats. A bolus dose of 50mg/kg-beryllium nitrate was administered singly followed by chelation therapy with GSH, DMPS + Se and DPA + Se at various durations of 1,3 and 7 days respectively. Results revealed a significant fall in the glycogen content, whereas, a marginal fall in the protein was also observed. The enzymatic activity of alkaline phosphatase and adenosine triphosphatase was depleted; on the contrary, there was a significant rise in the acid phosphatase and glucose-6-phosphatase pattern. A rise in the hepatic lipid peroxidation activity is a direct indication of oxidative damage resulting in free radical generation. The distribution of the metal by atomic absorption spectrophotometry revealed an increased concentration of beryllium in liver and kidney, followed by lung and uterus. The relative ability of three chelating agents to act as antagonists, for acute beryllium poisoning, have been examined in liver, kidney, lungs and uterus. The appreciable change in the beryllium concentration in various organs is duration dependent during the entire period being highly significant at 7 days regimen. Biochemical and distribution studies reveal that DPA + Se was the most effective therapeutic agent followed by DMPS + Se and GSH.
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PMID:Role of chelating agents and antioxidants in beryllium induced toxicity. 1262 5

The ever-increasing understanding of oxygen radical-linked diseases, including the biological process of aging, has stimulated general interest in modulating these biological events. Melatonin has been reported to have antioxidant properties in addition to its known hormonal activities. However, reports on low-level chronic administration with its anti-aging influence are scanty. Hence, the present study was aimed to investigate the influence of low-dose chronic administration (0.10 mg/kg body weight/day for 3 months) of melatonin against age-induced oxidative stress in mice tissues, namely brain, liver, spleen and kidney. Sixteen-month-old mice were supplemented with melatonin (0.10 mg/kg body weight/day) for three months and then autopsied (at the age of 19 months) for the biochemical estimation of lipid peroxidation, reduced glutathione (GSH), glutathione disulphide (GSSG), glutathione peroxidase (GSH-Px) and serum phosphatase activity. Results indicate that age-induced augmentation (compared to 6-8-week-old mice) in the level of lipid peroxidation, GSSG and acid phosphatase is significantly (P < 0.001) ameliorated in melatonin-treated mice. Age-induced decline in the level of GSH, GSH-Px and alkaline phosphatase activity is inhibited significantly by the long-term administration of melatonin. The findings indicate that low-dose chronic administration of melatonin acts as a free radical scavenger and anti-aging agent.
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PMID:Melatonin-induced reduction in age-related accumulation of oxidative damage in mice. 1281 12

The oral administration of Mentha extract (ME) before exposure to gamma radiation was found to be effective in increasing the frequency of radiation-induced endogenous spleen colonies. A significant increase in the weight of the spleen was observed in animals of the Mentha and radiation combined group in comparison to the irradiation-alone group on day 10 of postirradiation. Furthermore, a significant increase in the body weight of animals in the Mentha and radiation combined group was observed in all the radiation doses studied. A regression analysis of survival data yielded LD50/30 as 6.48 +/- 0.07 and 11.59 +/- 0.21 Gy for the irradiation-alone and the Mentha and radiation combined group, respectively, and produced a dose reduction factor (DRF) of 1.78. Significant increases in total erythrocyte and leucocyte counts, hemoglobin concentration, and hematocrit values were observed in the animals of the Mentha and radiation combined group in comparison to the hematological values observed in the irradiation-alone group at all radiation doses studied (6, 8, and 10 Gy). A dose-dependent decrease in reduced glutathione (GSH) content and an increase in lipid peroxidation (LPO) levels were observed in control animals. However, the animals of the Mentha and radiation combined group exhibited a significant increase in GSH content and a decrease in LPO level, but the values remained below normal. A significant increase in the serum alkaline phosphatase activity was observed in the animals of the Mentha and radiation combined group during the entire period of study, and normal range was evident at 24 h (6 Gy) and day 5 (8 Gy). However, this level could not be restored even at day 30 in 10 Gy exposed animals. Measured acid phosphatase activity in the animals of the Mentha and radiation combined group was found to be significantly lower than the respective controls and attained normal value at day 5 (6 and 8 Gy) and day 20 (10 Gy).
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PMID:Radioprotection of Swiss albino mice by plant extract Mentha piperita (Linn.). 1367 38


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