摘要:

A short-term evaluation of 6 months of estrogen therapy on oxidant status in 38 postmenopausal women was conducted. The levels of serum lipid peroxidation products, glutathione (GSH) status, and glutathione-related enzymes were evaluated before and after 6 months of hormone replacement therapy. After 6 months of estrogen treatment there was a significantly increased concentration of thiobarbituric acid-reactive substances (TBARS), which are an end product of lipid peroxidation. This was accompanied by a significant increase in the activity of glutathione peroxidase (GSH-Px). However, the activities of glutathione reductase (GSSG-R) and superoxide dism utase (SOD) were significantly decreased and total protein thiols were reduced. Data suggest that hormone replacement therapy in postmenopausal women is associated with oxidant mechanisms.

ISSN:1528-7394    

DOI:10.1080/009841000157023

出版商:Informa UK Ltd    

年代:2000

数据来源: Taylor

摘要:

Oxidative stress was compared in plasm a of 15 recently diagnosed (<2 mo) or 15 longstanding (>5 yr) type 1 diabetic patients with 15 healthy volunteers. Lipid peroxidation indices measured in plasma included thiobarbituric acid-reactive substances (TBARS), conjugated dienes, and lipid hydroperoxide (ROOH). The values obtained were corrected for phospholipid to minimize this as a confounding factor. In recently diagnosed diabetics, plasm a conjugated lipid dienes were significantly elevated. However, in longstanding diabetics there was a marked increase in TBARS, conjugated dienes, and lipid hydroperoxide levels. Our findings showed increased oxidative stress in type 1 diabetics regardless of metabolic control and that conjugated diene measurement appeared to be the most sensitive bioindicator of oxidant stress in our population.

ISSN:1528-7394    

DOI:10.1080/009841000157032

出版商:Informa UK Ltd    

年代:2000

数据来源: Taylor

摘要:

Recent epidemiological studies proposed that glutathione S-transferase (GST) T1 null genotype was correlated with an increased susceptibility to diseases associated with oxidative stress, including cancer. A comparative study using erythrocytes from individuals with GSTT1 null genotype was carried out to determine how resistance to oxidative stress is affected by lack of this gene, and whether the GST status of a person is an important factor in risk toward oxidant chemicals. Malondialdehyde and carbonyl levels and fluorescence and chemilum inescence formation were used as biomarkers of oxidative stress in erythrocytes exposed in vitro to cumene hydroperoxide (CumOOH), an oxidizing agent. When peroxidation-dependent changes in these parameters were compared between GSTT1 null genotype and controls, who are both GSTM1 and GSTT1 positive, no significant differences were found between the two genotypes, although the erythrocytes of the GSTT1 null group had lower GSTT1 activity toward Cum OOH. Our results indicate that erythrocytes from individuals with GSTT1 null genotype are not abnorm ally susceptible to CumOOH-induced oxidant challenge.

ISSN:1528-7394    

DOI:10.1080/009841000157041

出版商:Informa UK Ltd    

年代:2000

数据来源: Taylor

摘要:

Daily indium chloride doses of control (0), 50, 100, 200, or 400 mg/kg were administered orally to Sprague-Dawley rats by gavage, on d 6-15 of gestation, and daily metal doses of control (0), 50, 100, or 200 mg/kg were administered to New Zealand rabbits on d 6-20 of gestation. Further groups of pregnant rats were treated with control (0) or 400 mg/kg indium chloride orally on one of d 8, 9, 10, 11, 12, 13, 14, or 15 of gestation. The dams and fetuses were examined on d 21 (rats) and 30 (rabbits) of gestation, using standard teratological methods. Indium concentration was determined in the maternal and fetal blood, as well as in the amniotic fluid, by atomic absorption spectrometry. Indium was found to cross the placenta and appeared in fetal blood in proportion to the metal concentration of the maternal blood. In the amniotic fluid, indium concentrations remained below the detection limit. In rats, indium chloride produced dose-dependent maternal toxic effects, with a dose of 400 mg/kg inducing embryotoxicity (embryolethality) and teratogenicity. Doses of 200 and 100 mg/kg were embryotoxic (retarding) and teratogenic, causing skeletal and visceral anomalies in addition to external anomalies (rudimentary or missing tail, syndactylia, clubfoot, exencephalia) in rats. In rabbits, 200 mg/kg indium chloride was lethal for the dams and the embryos (some of the animals died, and the number of abortions and full resorptions increased). This dose was found to be teratogenic (caused gross renal anomalies) and increased the frequency of fetuses with skeletal retardation. In rats, the effects of indium chloride causing fetal retardation was found to be independent of exposure time. The teratogenic effects were the highest on d 11 and 12 of gestation, when indium chloride caused gross external malformations. Data suggest that the teratogenic effects of indium chloride can be attributed primarily to a direct cytotoxic action of indium resulting from placental transfer, but the effect is not a selective one, as it appears only in the presence of maternal toxic effects.

ISSN:1528-7394    

DOI:10.1080/009841000157050

出版商:Informa UK Ltd    

年代:2000

数据来源: Taylor

摘要:

The following hypotheses were examined using Pekin ducks (Anas platyrhynchos) as a model for marine ducks: cadmium (Cd) intake affects (1) salt gland and/or kidney function of ducks and (2) osmoregulation differently in male and female ducks. Birds were fed 0, 50, or 300 mug Cd/g food. They were gradually acclimated to 450 m M NaCl and then drank 300 m M NaCl for 3 mo while salt gland secretion (SGS), glomerular filtration rate (GFR), total body water (TBW), and water flux (WF) were measured in ducks eating control and high-Cd diets. Cadmium ingestion did not markedly affect body mass, but significantly enlarged the salt glands and kidneys. Enhancement of kidney mass was greater in males. Cadmium ingestion did not affect TBW or WF, but tended to increase interstitial fluid space at the expense of intracellular fluid. Sex did not affect TBW, but males had greater WF. Birds that ate Cd diets, especially the higher Cd diet, exhibited renal tubular damage and lower GFR. Ducks that ate Cd had lower plasma sodium concentration and osmolality and, to activate SGS, required longer infusion of NaCl and larger increments in extracellular osmolality and volume. Cadmium ingestion did not affect SGS rate or [Na+]. Both hypotheses were accepted since birds that ate Cd had lower GFR and delayed onset of SGS in response to salt challenge and the effects of Cd on the size and response of excretory organs were sexually disparate. Cadmium appeared to compromise the salt excretion of Pekin ducks. However, they are less salt tolerant than seaducks and, in this study, had higher organ Cd concentrations than those seen in wild ducks. Further studies are needed to determine if these observations also apply to the more salt-tolerant seaducks.

ISSN:1528-7394    

DOI:10.1080/009841000157069

出版商:Informa UK Ltd    

年代:2000

数据来源: Taylor

摘要:

Organophosphorous (OP) insecticide-induced inhibition and oxime reactivation of acetylcholinesterase (AChE) was determined in whole-brain homogenates prepared from 15-d-old chick embryos. Doses of chlorpyrifos, parathion, acephate, and trichlorfon that inhibited AChE>70% were administered to the embryos. Following insecticide exposure, an in vitro system compared the capability of the oximes pralidoxime (2-PAM), obidoxime, TMB-4, and HI-6 to reactivate the OP-inhibited AChE. Concentration-related increases in AChE activities were noted in embryo brains reactivated with 2-PAM, TMB, and HI-6.2-PAM was the most effective reactivator of trichlorfon-inhibited AChE; 2-PAM and obidoxime were relatively similar in effectiveness for reactivation of AChE inhibited with the other OP insecticides used as test agents. All oximes were similarly effective against acephate, but HI-6 was the least effective reactivator of AChE in chick embryo brain homogenates inhibited by the other OP insecticides. These results suggest that both the OP insecticide inhibiting AChE and the oxime reactivating this enzyme can contribute to the effectiveness of the avian brain AChE reactivation.

ISSN:1528-7394    

DOI:10.1080/009841000157078

出版商:Informa UK Ltd    

年代:2000

数据来源: Taylor