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Modulatory effect of henna leaf (Lawsonia inermis) on drug metabolising phase I and phase II enzymes, antioxidant enzymes, lipid peroxidation and chemically induced skin and forestomach papillomagenesis in mice.

Henna leaf (Lawsonia inermis), commonly known as Mehndi is cultivated throughout India and is a very popular natural dye to color hand and hair. It is an integral part of indigenous culture, and is also known for its medicinal value. The effect of 200 and 400 mg/kg body weight of 80% ethanolic extract of the fresh leaves of Lawsonia inermis were examined on drug metabolizing phase-I and phase-II enzymes, antioxidant enzymes, glutathione content, lactate dehydrogenase and lipid peroxidation in the liver of 7 weeks old Swiss albino mice. Also anticarcinogenic potential of Henna leaf extract was studied adopting the protocol of benzo(a)pyrene induced forestomach and 7,12 dimethylbenz(a)anthracene (DMBA)-initiated and croton oil-promoted skin papillomagenesis. Our primary findings reveal the 'duel-acting' nature of henna leaf as deduced from its potential to induce only the phase-II enzyme activity, associated mainly with carcinogen detoxification in liver of mice and inhibit the phase I enzyme activities. The hepatic glutathione S-transferase and DT-diaphorase specific activities were elevated above basal (p < 0.005) level by Lawsonia inermis extract treatment. With reference to antioxidant enzymes the investigated doses were effective in increasing the hepatic glutathione reductase (GR), superoxide dismutase (SOD) and catalase activities significantly (from p < 0.05 to p < 0.005) at both the dose levels. Reduced glutathione (GSH) measured as non-protein sulphydryl was found to be significantly elevated in liver (p < 0.005) and in all the extrahepatic organs studied (from p < 0.05 to p < 0.005). Among the extrahepatic organs examined (forestomach, kidney and lung) glutathione S-transferase and DT-diaphorase level were increased in a dose independent manner (from p < 0.05 to p < 0.005). Chemopreventive response was measured by the average number of papillomas per mouse (tumor burden) as well as percentage of tumor bearing animals and tumor multiplicity. There was a significant inhibition of tumor burden in both the tumor model systems studied (from p < 0.01 to p < 0.001). Tumor incidence was also reduced by both the doses used in our experiment in both the model systems.

Animals↗

Schistosoma mansoni: the developmental regulation and immunolocalization of antioxidant enzymes.

Antioxidant enzymes from S. mansoni, cytosolic Cu-Zn superoxide dismutase (CT-SOD), signal-peptide-containing SOD (SP-SOD), glutathione peroxidase (GPX), and glutathione transferase (GST) were compared for their relative levels of transcript expression throughout development in a semiquantitative reverse transcriptase-polymerase chain reaction assay. All of the antioxidant enzymes exhibited a similar pattern of developmental regulation. Adult worms have the highest level of specific mRNA compared with larval stages. GST shows the highest level of expression, being approximately 10-fold more abundant than CT-SOD and SP-SOD and 100-fold more abundant than GPX. This order of expression was nearly consistent for all the developmental stages studied. To localize the antioxidant enzymes, immunofluorescence staining was performed on 3-hr schistosomula and adult worms. GPX, SP-SOD, and CT-SOD were all found to be associated with the adult tegument and gut epithelium. SP-SOD was also associated with organelle and cell membranes of parenchymal cells and interestingly with the spines of adult worms. Schistosomula, on the other hand, showed little immunofluorescence. These studies further demonstrate the developmental regulation of antioxidant enzymes and localize them to the host-parasite interface, supporting the notion that they have a role in allowing adult worms to evade immune attack.

Animals↗

Pre-exercise antioxidant enzyme activities determine the antioxidant enzyme erythrocyte response to exercise.

Free radical production increases during exercise and oxidative damage occurs in several tissues. We examined the effects of three different exercise tests on the pattern of change of erythrocyte enzyme antioxidant activities. The tests were a short maximal exercise test, a submaximal prolonged exercise test and a cycling stage during competition. The participants were amateur and professional cyclists with different training statuses and different basal erythrocyte antioxidant enzyme activities. The maximal test produced no changes in the erythrocyte antioxidant enzyme activities of amateur sportsmen. The submaximal test, performed at 80% of maximal oxygen uptake, decreased erythrocyte catalase (12%), glutathione peroxidase determined with H2O2 (14%) and glutathione reductase (16%); superoxide dismutase activity increased by about 25%. The cycling stage performed by professional cyclists increased erythrocyte catalase (29%) and glutathione reductase (10%) activities. The in vivo changes in glutathione reductase activity were confirmed by in vitro measurements: hydrogen peroxide decreased and the presence of catalase increased the activity of this enzyme. In conclusion, we suggest that the different erythrocyte antioxidant enzyme responses to diverse exercise tests can be explained by the effects of hydrogen peroxide and the superoxide anion on the antioxidant enzyme activities in erythrocytes.

Adult↗

Modulatory effect of Urtica dioica L. (Urticaceae) leaf extract on biotransformation enzyme systems, antioxidant enzymes, lactate dehydrogenase and lipid peroxidation in mice.

The effects of two doses (50 and 100 mg/kg body wt given orally for 14 days) of an ethanol-water (80%-20%) extract of Urtica dioica L. and butylated hydroxyanisole (BHA) were investigated, for phase I and phase II enzymes, antioxidant enzymes, lactate dehydrogenase, lipid peroxidation and sulfhydryl groups in the liver of Swiss albino mice (8-9 weeks old). A modulatory effect of two doses and BHA was also observed for the activities of glutathione S-transferase, DT-diaphorase, superoxide dismutase and catalase in the kidney, lung and forestomach, as compared with the control group. The activities of cytochrome b5 (cyt b5), NADH-cytochrome b5 reductase (cyt b5 R), glutathione S-transferase (GST), DT-diaphorase (DTD), glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD) and catalase (CAT) showed a significant increase in the liver at both dose levels of extract. Both extract-treated showed significantly lower activity of cytochrome P450 (cyt P450), lactate dehydrogenase (LDH), NADPH-cytochrome P450 reductase (cyt P450 R), total sulfhydryl groups (T-SH), nonprotein sulfhydryl groups (NP-SH) and protein-bound sulfhydryl groups (PB-SH). BHA-treated Swiss albino mice showed a notable increase in levels of cyt b5, DTD, T-SH, PB-SH, GPx, GR, and SOD in the liver while, LDH, cyt P450, cyt P450 R, Cyt b5 R, GST, NP-SH, and CAT levels were reduced significantly as compared to control values. The extract was effective in inducing GST, DTD, SOD and CAT activity in the forestomach and SOD and CAT activity in the lung at both dose levels. BHA-treated Swiss albino mice induced DTD, GST and all antioxidative parameters in the kidney, lung and forestomach.

Animals↗

The inhibitory effects of polychlorinated biphenyl Aroclor 1254 on Leydig cell LH receptors, steroidogenic enzymes and antioxidant enzymes in adult rats.

Polychlorinated biphenyls (PCBs) are global pollutants of major concern to human and animal reproductive health. The present study has examined the impact of Aroclor 1254 exposure on oxidative stress and testicular Leydig cell function. Adult albino male rats of the Wistar strain were dosed for 30 days with daily intraperitoneal injections of 2 mg/kg Aroclor 1254 or vehicle (corn oil). One day after the last treatment, animals were euthanized and blood collected for the assay of serum testosterone and estradiol. Testes were removed and Leydig cells were isolated for the assay of luteinizing hormone (LH) receptors, steroidogenic enzymes cytochrome P450 side chain cleavage enzyme (P450 scc), 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and 17beta-hydroxysteroid dehydrogenase (17beta-HSD). Cellular antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR), and glutathione-S-transferase (GST) were also assayed. Lipid peroxidation (LPO) and reactive oxygen species (ROS) were quantified. Results showed that Aroclor 1254 exposure lowered serum testosterone and estradiol levels. Leydig cell LH receptor density, activities of the steroidogenic enzymes P450 scc, 3beta-HSD, 17beta-HSD, antioxidant enzymes SOD, CAT, GPX, GR, and GST were significantly diminished whereas, LPO and ROS significantly elevated. Taken together, these results suggest that inefficient LH receptors, steroidogenic enzymes and antioxidant enzymes are possible mechanisms by which Aroclor 1254 treatment disrupts Leydig cell steroidogenesis.

Animals↗

Role of antioxidant enzymes and antioxidant compound probucol in antiradical protection of pancreatic beta-cells during alloxan-induced diabetes.

The severity of disturbances in carbohydrate metabolism in rats with alloxan-induced diabetes depended on activity of antioxidant enzymes in the target organ (pancreas). Damage to the pancreas is related to intensive generation of reactive oxygen species, free radicals, and lipid peroxides. Alloxan-induced diabetes in rats is a free radical disease, which in vivo serves as a useful model for the search for pharmacological preparations with antiradical and antioxidant properties. The antioxidant compound probucol indirectly increased activity of antioxidant enzymes in the pancreas and prevented the development of alloxan-induced diabetes in rats. Our results indicate that different sensitivity of laboratory animals of various species (rats and guinea pigs) to the influence of alloxan is associated with abnormal variations in activity of enzymes utilizing reactive oxygen species and lipid peroxides in mammalian pancreatic cells.

Animals↗

Effect of exogenous antioxidant enzymes and antioxidants on the development of endotoxin-induced hepatocellular necrosis in rats.

To determine whether released oxidants in endotoxemia contribute to the development of hepatocellular necrosis, we examined the effects of antioxidants and antioxidant enzymes on endotoxin hepatotoxicity in rats. In rats given endotoxin, focal and random hepatocellular coagulative necrotic areas with infiltration of polymorphonuclear leukocytes and mononuclear cells and an elevation of serum transaminase activities were found. The extent of hepatocellular necrosis and the level of serum transaminase activities were not significantly decreased by treatment with superoxide dismutase, catalase, alpha-tocopherol or allopurinol. These experimental data indicate that even if endotoxin is related to a release of oxidants, the oxidants do not appear to play an important role in the development of hepatocellular necrosis.

Allopurinol↗

Effects of leucocyanidines on activities of metabolizing enzymes and antioxidant enzymes.

Procyanidolic oligomers (leucocyanidines, LCs) extracted from grape seeds (Vitis vinifera) are known to have antioxidant and antimutagenic activities, and a protective effect against cardiovascular disease. In the present study we examined the influence of LCs on the activities of phase 1 enzymes and conjugation enzymes and on antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. Administration of LCs (25, 50, and 100 mg/kg. p.o. for 7 d) markedly decreased the activities of NADPH-cytochrome P450 reductase, P4501A1, P4501A2, and P4503A4, but significantly increased the activities of glutathione S-transferase and phenolsulfotransferase in rat liver. However, the activities of antioxidant enzymes were not affected by LC administration. The inhibition of P450s and increases in phase II enzyme activities indicate a role for LCs as a chemopreventive agent against toxic or carcinogenic metabolites of P450 isozymes.

Animals↗

Elevated levels of DNA repair enzymes and antioxidative enzymes by (+)-catechin in murine microglia cells after oxidative stress.

(+)-Catechin possesses a broad range of pharmacological properties, including antioxidative effect. However, little is reported on the mechanism by which (+)-catechin protects microglia cells from DNA damage by oxidative stress. In this study, TUNEL assay and DNA electrophorysis indicated that (+)-catechin markedly blocked DNA fragmentation and apoptosis of microglia cells by tBHP exposure. A potent antioxidative effect of (+)-catechin was confirmed by comparison with a putative antioxidant agent, N-acetylcysteine at the lower doses. Furthermore, the increased intracellular ROS by tBHP exposure were scavenged by elevated activities of catalase (CAT) and superoxide dismutase (SOD) after (+)-catechin treatment. (+)-Catechin partially inhibited the activation of caspase-3, thereby both cleavage of poly (ADP-ribose) polymerase (PARP) and degradation of inhibitor of caspase-activated DNase (ICAD) were effectively abolished. In addition, the expression of PARP for repair of impaired DNA was significantly increased by (+)-catechin treatment. Taken together, these data suggest that protective effects of (+)-catechin against oxidative DNA damage of microglia cells is exerted by the increased expression of DNA repair enzyme PARP and antioxidant enzyme activities.

Animals↗

Focus on antioxidant enzymes and antioxidant strategies in smoking related airway diseases.

Cigarette smoke causes significant oxidant stress which is further enhanced by recruitment and activation of inflammatory cells to the lung. Polymorphisms in some detoxification enzymes are thought to increase the risk of developing chronic obstructive pulmonary disease (COPD), but the ultimate role of genetic variability in antioxidant and/or detoxification enzymes in COPD remains obscure. Some antioxidant enzymes are inducted, but the extent of induction is insufficient to protect the lung/alveolar epithelium against cigarette smoke. Exogenous antioxidants such as vitamins do not seem to protect against cigarette smoke related lung injury. Glutathione related synthetic drugs such as N-acetylcysteine have shown some benefits, but they may have pro-oxidant side effects. Synthetic compounds with superoxide dismutase and catalase activities have shown promising results in animal models against a variety of oxidant exposures including cigarette smoke in the lung. These results are in agreement with studies highlighting the importance of alveolar antioxidant protection mechanisms in oxidant stress and their inducibility. These new drugs need to be tested in cigarette smoking related lung injury/inflammation since inflammation/oxidant stress can continue after discontinuation of smoking.

Antioxidants↗

Effects of peroxisome proliferators on antioxidant enzymes and antioxidant vitamins in rats and hamsters.

Peroxisome proliferators (PPs) cause hepatomegaly, peroxisome proliferation, and hepatocarcinogenesis in rats and mice, whereas hamsters are less responsive to PPs. PPs increase the activities of enzymes involved in peroxisomal beta-oxidation and omega-hydroxylation of fatty acids, which has been hypothesized to result in oxidative stress. The hypothesis of this study was that differential modulation of antioxidant enzymes and vitamins might account for differences in species susceptibility to PPs. Accordingly, we measured the activities of DT-diaphorase and superoxide dismutase (SOD) and the hepatic content of ascorbic acid and alpha-tocopherol in male Sprague-Dawley rats and Syrian hamsters fed 2 doses of 3 known peroxisome proliferators (dibutyl phthalate [DBP], gemfibrozil, and [4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio]acetic acid (Wy-14,643) for 6, 34, or 90 days. In untreated animals, the activity of DT-diaphorase was much higher in hamsters than in rats, but the control levels of SOD, ascorbic acid and alpha-tocopherol were similar. In rats and hamsters treated with Wy-14,643, we observed decreases in alpha-tocopherol content and total SOD activity. DT-diaphorase was decreased in activity following Wy-14,643 treatment in rats at all time points and doses, but only sporadically affected in hamsters. Rats and hamsters treated with DBP demonstrated increased SOD activity at 6 days; however, in the rat, DBP decreased SOD activity at 90 days and alpha-tocopherol content was decreased throughout. In gemfibrozil treated rats and hamsters, a decrease in alpha-tocopherol content and an increase in DT-diaphorase activity were observed. In either species, no consistent trend was observed in total ascorbic acid content after treatment with any of the PPs. In conclusion, these data suggest that both rats and hamsters are compromised in antioxidant capabilities following PP treatment and additional hypotheses for species susceptibility should be considered.

Animals↗

Chemomodulatory efficacy of basil leaf (Ocimum basilicum) on drug metabolizing and antioxidant enzymes, and on carcinogen-induced skin and forestomach papillomagenesis.

Basil or sweet basil (Ocimum basilicum) is cultivated throughout India and is known for its medicinal value. The effects of doses of 200 and 400 mg/kg body weight of hydroalcoholic extract (80% ethanol, 20% water) of the fresh leaves of Ocimum basilicum on xenobiotic metabolizing Phase I and Phase II enzymes, antioxidant enzymes, Glutathione content, Lactate dehydrogenase and lipid peroxidation in the liver of 8-9 weeks old Swiss albino mice were examined. Furthermore, the anticarcinogenic potential of basil leaf extract was studied, using the model of Benzo(a)pyrene-induced forestomach and 7,12 dimethyl benz(a)anthracene (DMBA)-initiated skin papillomagenesis. The hepatic glutathione S-transferase and DT-diaphorase specific activities were elevated above basal level by basil leaf treatment (from p < 0.005 to p < 0.001). Basil leaf extract was very effective in elevating antioxidant enzyme response by increasing significantly the hepatic glutathione reductase (GR) (p < 0.005), superoxide dismutase (SOD) (p < 0.05), and catalase activities (p < 0.005). Reduced glutathione (GSH), the major intracellular antioxidant, showed a significant elevation in the liver (p < 0.005) and also in all the extrahepatic organs (from p < 0.05 to p < 0.005). In the forestomach, kidney and lung, glutathione S-transferase and DT-diaphorase levels were augmented significantly, varying from p < 0.01 to p < 0.001. There were significant decreases in lipid peroxidation and lactate dehydrogenase activity. Chemopreventive response was evident from the reduced tumor burden (the average number of papillomas/mouse, p < 0.005 to p < 0.001), as well as from the reduced percentage of tumor bearing-animals. Basil leaf, as deduced from the results, augmented mainly the Phase II enzyme activity that is associated with detoxification of xenobiotics, while inhibiting the Phase I enzyme activity. There was an induction in antioxidant level that correlates with the significant reduction of lipid peroxidation and lactate dehydrogenase formation. Moreover, Basil leaf extract was highly effective in inhibiting carcinogen-induced tumor incidence in both the tumor models at peri-initiational level.

9,10-Dimethyl-1,2-benzanthracene↗

Response of blood cell antioxidant enzyme defences to antioxidant diet supplementation and to intense exercise.

BACKGROUND: Exhaustive exercise induces oxidative stress. The cellular antioxidant defence systems have demonstrated great adaptation to chronic exercise. AIM: To establish the influence of the antioxidant diet supplementation on the erythrocyte and lymphocyte antioxidant enzyme activities in athletes at basal and post-exercise levels. METHODS: Fifteen amateur trained male athletes were randomly distributed in two groups: control and antioxidant supplemented (90 days' diet supplementation with 500 mg/day vitamin E and 30 mg/day beta-carotene, and the last 15 days also with 1 g/day vitamin C). The study was double blind. Maximal and submaximal exercise tests were performed after three months of diet supplementation. The study was developed during the training and competition season. RESULTS: The sportsmen of the supplemented group presented significantly higher plasmatic final levels of vitamin C, vitamin E and beta-carotene. Erythrocyte glutathione reductase activity significantly decreased in the placebo group but was maintained in the supplemented group after the three months studied. The erythrocyte superoxide dismutase activity increased after the training/competition period in the placebo group. Lymphocyte catalase and glutathione peroxidase activities increased significantly in the supplemented group after the supplementation period but were maintained in the placebo group. No effects of the antioxidant supplementation were observed in the erythrocyte antioxidant enzyme response to the exercise tests. The antioxidant supplementation induced a better adaptation of lymphocyte catalase after submaximal test. CONCLUSIONS: Lymphocytes showed higher sensibility to antioxidant supplementation, improving the response of antioxidant enzymes to training and to acute exercise. In erythrocytes the training adaptations were more important than the antioxidant supplementation effects.

Adaptation, Physiological↗

Cerebral enzyme antioxidant system. Influence of aging and phosphatidylcholine.

To obtain a comprehensive profile of the age-related changes of the antioxidant enzyme system in discrete brain regions (cortex, caudate-putamen, substantia nigra, thalamus), the present study involved practically the total life span of male Wistar rats (from 5 to 35 months of age). The activities of both glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase increase from 5 to 25 months of life and remain relatively constant or decrease scantily thereafter. In thalamus, the activity of total superoxide dismutase (SOD) increases from 5 to 20 months of rat life and decreases thereafter. Conversely, in both substantia nigra and caudate-putamen, enzyme activity declines steadily with age, while in parietotemporal cortex enzyme activity deteriorates from the 25th month onward. In both caudate-putamen and parietotemporal cortex, the activity of glutathione peroxidase increases from 5 to 20 months of life and remains relatively constant thereafter, while in substantia nigra the enzyme activity is practically unmodified during the life span. Furthermore, the activity of glutathione reductase in parietotemporal cortex declines from the 20th month onward, while in caudate-putamen and thalamus, enzyme activity deteriorates after an increase from 5 to 20 months of life. The interference of phosphatidylcholine and/or its metabolite(s) with the cerebral enzyme antioxidant system shows a characteristic specificity as regards both the time of onset and the enzyme activities involved, namely, SOD and glutathione reductase. The interference with SOD is related to the cytosolic form of the enzyme and affects the cortex only of 5-month-old animals and also extends to the thalamus of 15-month-old rats and all regions in 25-month-old ones.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

Decreased expression of antioxidant enzymes and increased expression of chemokines in COPD lung.

The involvement of inflammation in the pathogenesis of chronic obstructive pulmonary disease (COPD) has been investigated using samples from relatively central airways such as airway biopsies, but there have been fewer studies in the peripheral lung, which is thought to be the main site of the disease process. To determine the molecules that relate to the mechanisms underlying the pathogenesis of COPD, we evaluated the mRNA expression of inflammatory cytokines, chemokines, oxidant enzymes, antioxidant enzymes, proteinases and antiproteinases in peripheral lung tissues from 33 COPD and non-COPD subjects who were undergoing lung resection for lung cancer using an RT-PCR technique. Among the 42 studied candidate genes, the expressions of mRNA for catalase, glutathion S-transferase P1 (GSTP1), glutathion S-transferase M1 (GSTM1), microsomal epoxide hydrolase (mEPHX) and tissue inhibitor of metalloproteinase 2 (TIMP2) were significantly decreased in COPD lung tissues compared with those in non-COPD tissues, and most of these decreases were significantly correlated with the degree of airflow limitation. On the other hand, the expressions of mRNA for interleukin 1beta (IL-1beta), interleukin 8 (IL-8), growth-related oncogene-alpha (Gro-alpha) and monocyte chemotactic protein-1 (MCP-1) were significantly increased in COPD lungs. Most of these changes were also associated with cigarette smoking. These data suggest that an impairment of protective mechanisms against oxidants and xenobiotics, in addition to the upregulation of CXC- and CC-chemokines, may be associated with cigarette smoking and involved in the inflammatory process of COPD.

Aged↗

Effect of selenium on N-nitrosodiethylamine-induced multistage hepatocarcinogenesis with reference to lipid peroxidation and enzymic antioxidants.

We have studied the relationship between antioxidant and anticancer properties of selenium (Se) in multistage hepatocarcinogenesis induced by N-nitrosodiethylamine (DEN). In this study we have observed an increased level of lipid peroxide (LPO) products and decreased antioxidant enzyme activities (superoxide dismutase and catalase) in hepatoma and surrounding liver tissues of cancer-bearing animals. Selenium (Se) was supplemented either before initiation or during initiation and selection/promotion phases of hepatocarcinogenesis and was found to be effective in altering hepatic lipid peroxidation and antioxidant enzyme activities to a statistically significant level measured either in the hepatoma or in the surrounding liver tissues. These alterations inclined towards normal in a time-dependent manner on selenium supplementation. Furthermore, increased levels of lipid peroxidation and decreased levels of antioxidants (superoxide dismutase and catalase) were also observed in distant organs of cancer-bearing rats other than the tumour-bearing site. These alterations are brought back to normal levels upon Se treatment. Our results confirm the fact that Se is particularly protective in limiting the action of DEN by its antioxidant property.

Alkylating Agents↗

Failure of premature rabbits to increase lung antioxidant enzyme activities after hyperoxic exposure: antioxidant enzyme gene expression and pharmacologic intervention with endotoxin and dexamethasone.

Premature rabbits, unlike full-term rabbits, are unable to mount a protective increase in pulmonary antioxidant enzyme (AOE) activities in response to 48 h of hyperoxic exposure and demonstrate increased pulmonary O2 toxicity compared with full-term rabbits. To examine AOE gene expression of CuZn superoxide dismutase (SOD), Mn SOD, catalase, and glutathione peroxidase in preterm versus term rabbits in response to hyperoxia, 29.5 d preterm rabbits (delivered by hysterotomy) and term rabbits (spontaneously vaginally delivered) were exposed to 48 h of > 90% O2 or room air. Preterm rabbits had a significant increase in CuZn SOD mRNA without corresponding AOE activity increases, suggesting translational/posttranslational inhibition. In full-term rabbits, the magnitude of lung AOE mRNA changes was associated with concordant magnitude changes in activities of CuZn SOD, Mn SOD, and catalase, suggesting pretranslational regulation of AOE gene expression; glutathione peroxidase, however, appears to be regulated translationally/posttranslationally. To investigate potential pharmacologic means of overcoming the susceptibility of the preterm rabbit to O2 toxicity, 29.5 d preterm rabbits received 20-40 micrograms/kg of Salmonella typhimurium endotoxin or diluent S.C. (after birth and at 24 h); in separate experiments, pregnant rabbits received intramuscular injections of dexamethasone (0.01-0.05 mg/kg) or saline on gestational d 27.5 and 28.5 and underwent hysterotomy at 29.5 d.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗