Light and electron microscopical changes in the liver of mice following treatment with aminotriazole

Reitze, H. K.; Seitz, Karl‐August

doi:10.1016/s0232-1513(85)80053-0

Cited by 9 publications

(2 citation statements)

References 28 publications

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“…This is further supported by the fact that a 90% increase in concentration of inorganic peroxides (mainly H,02) has been found in young houseflies chronically drinking AT (Allen et al 1983). Thus, tissue increases of H20, can be one of the principal causes of many deleterious changes reported in AT-treated animals (Jones & Neil 1982;Reitze & Seitz 1985).…”

Section: U Lungmentioning

confidence: 76%

Aminotriazole Effects on Lung and Heart H₂O₂ Detoxifying Enzymes and TBA‐RS at Two pO₂

López-Torres

Pérez‐Campo

Quiroga

1990

Pharmacology & Toxicology

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In order to clarify the physiological role in vivo of H2O2-detoxifying enzymes at low and high levels of O2 tension we studied catalase (CAT), glutathione peroxidases (GP), and in vivo peroxidation (TBA-RS) in the lung and heart of Rana perezi frogs chronically treated with hyperoxia, aminotriazole (AT) -a CAT inhibitor-, or both. Hyperoxia did not change CAT, GP or TBA-RS. Aminotriazole caused an almost complete depletion of CAT, a 30% decrease of GP and a 132% (lung) to 200% (heart) increase of TBA-RS. Changes similar to these were found in the group treated with AT in hyperoxia. No mortality or changes in total or organ weight occurred in the experimental groups. Main conclusions are: (1) The maximal hyperoxia tolerance showed by frogs among vertebrates does not need antioxidant enzyme induction from lung or heart and is probably related to the presence of high constitutive levels of GP in relation to metabolic rate. (2) Even in normoxia the tissues present significant amounts of H2O2, and CAT is needed to avoid oxidative damage. GP does not compensate its absence. The implications of these results in relation to oxygen toxicity in man is discussed.

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Section: U Lungmentioning

confidence: 76%

Aminotriazole Effects on Lung and Heart H₂O₂ Detoxifying Enzymes and TBA‐RS at Two pO₂

López-Torres

Pérez‐Campo

Quiroga

1990

Pharmacology & Toxicology

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“…Thus, AT has been shown to inhibit cytochrome P-450 (Handler et al, 1986) and fatty acid synthesis in the liver, as well as produce alterations in liver structures (Reitze and Seitz, 1985). Although these effects have not been shown in the brain, one cannot exclude other explanations concerning the nature of AT'S effects on ethanol-induced behaviors (Hunt, 1996).…”

mentioning

confidence: 99%

AcuteLead Acetate Administration Potentiates Ethanol‐Induced Locomotor Activity in Mice: The Role of Brain Catalase

Correa

Miquel

Sanchis‐Segura

et al. 1999

Alcoholism Clin & Exp Res

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It has been proposed that brain catalase plays a role in the modulation of some psychopharmacological effects of ethanol. The acute administration of lead acetate has demonstrated a transient increase in several antioxidant cell mechanisms, including catalase. In the present study, we investigated the effects of acute lead acetate administration on ethanol-induced behavior, brain catalase activity, and the relation between both effects. Lead acetate (100 mg/kg) or saline was injected intraperitoncally in mice. At different intervals of time (1, 3, 5, 7, 9, or 11 days) after this treatment, ethanol (2.5 g/kg) was injected intraperitoneally and the mice were placed in open field chambers. Results indicated that the locomotor activity induced by ethanol was significantly increased. Maximum ethanol-induced locomotion increase (70% more activity than control animals) was found in animals treated with lead acetate 7 days before ethanol administration. Total brain catalase activity in lead-pretreated animals also showed a significant induction, which was maximum 7 days after lead administration. A significant correlation was found between both effects of locomotor and catalase activity. In a second study, the effect of lead administration on d-amphetamine (2.0 mg/kg) and tert-butanol-(0.5 g/kg) induced locomotor activity was investigated. Lead acetate treatment did not affect the locomotion induced by these drugs. These data suggest that brain catalase is involved in ethanol's effects. They also provide further support for the notion that acetaldehyde may be produced directly in the brain via catalase and that it may be a factor mediating some of ethanol's central effects.

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Cyanamide reduces brain catalase and ethanol-induced locomotor activity: is there a functional link?

Sanchis‐Segura¹,

Miquel²,

Correa³

et al. 1999

Psychopharmacology

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The present study was designed in an attempt to assess a previously suggested role of brain catalase activity in ethanol-induced behaviour by examining ethanol-induced locomotor activity in cyanamide-treated mice. Mice were pretreated with IP injections of the catalase inhibitor cyanamide (3.75, 7.5, 15, 30 or 45 mg/kg) or saline. Following this treatment, animals in each group received IP injections of ethanol (0.0, 1.6, 2.4 or 3.2 g/kg) and locomotion was recorded. Several time intervals (0, 5, 10, 15, 20 or 25 h) between the two treatments were also evaluated. Results indicated that cyanamide administration produced a dose-dependent decrease in ethanol-induced locomotor activity that depends on the time between treatments. However, cyanamide did not change spontaneous or d-amphetamine-induced locomotor activity. Moreover, an additive effect of cyanamide and another brain catalase inhibitor, 3-amino-1,2,4-triazole (AT), on the reduction of ethanol-induced locomotor activity was observed. Perfused brain homogenates of mice treated with cyanamide, AT or cyanamide+AT showed a significant reduction of brain catalase activity. The dose and time patterns of both effects were closely related and a significant correlation between them was obtained. These results suggest that cyanamide could reduce locomotor activity through its inhibition of brain catalase, giving further support to the notion that brain catalase may be an important regulator of some ethanol-induced behavioural effects.

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Light and electron microscopical changes in the liver of mice following treatment with aminotriazole

Cited by 9 publications

References 28 publications

Aminotriazole Effects on Lung and Heart H₂O₂ Detoxifying Enzymes and TBA‐RS at Two pO₂

Aminotriazole Effects on Lung and Heart H₂O₂ Detoxifying Enzymes and TBA‐RS at Two pO₂

AcuteLead Acetate Administration Potentiates Ethanol‐Induced Locomotor Activity in Mice: The Role of Brain Catalase

Cyanamide reduces brain catalase and ethanol-induced locomotor activity: is there a functional link?

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Light and electron microscopical changes in the liver of mice following treatment with aminotriazole

Cited by 9 publications

References 28 publications

Aminotriazole Effects on Lung and Heart H2O2 Detoxifying Enzymes and TBA‐RS at Two pO2

Aminotriazole Effects on Lung and Heart H2O2 Detoxifying Enzymes and TBA‐RS at Two pO2

AcuteLead Acetate Administration Potentiates Ethanol‐Induced Locomotor Activity in Mice: The Role of Brain Catalase

Cyanamide reduces brain catalase and ethanol-induced locomotor activity: is there a functional link?

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Resources

About

Aminotriazole Effects on Lung and Heart H₂O₂ Detoxifying Enzymes and TBA‐RS at Two pO₂

Aminotriazole Effects on Lung and Heart H₂O₂ Detoxifying Enzymes and TBA‐RS at Two pO₂