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PubMed1983

[Changes in the oxidation-reduction system of glutathione--glutathione reductase [NAD(P). H] in the blood and tissues of white rats exposed to high and low temperatures].

The content of different forms of glutathione and the NADPH-dependent glutathione reductasa activity in blood, brain, liver and sceletal muscle of the white rats exposed to low and high temperatures have been investigated. It was shown that in general cooling of animals the amount of glutathione in blood, brain and liver increases, the glutathione reductasa [NAD(P)H] activity decreases. Under super-heating conditions concentration of all forms of glutathione in blood and tissues and the glutathione reductasa activity reduce. Data obtained permitted to assume the considerable role of the changes of the glutathione-glutathione reductasa system state in the realization of temperature factors action.

Animals↗
PubMed1985

Identification of a novel, thiol-containing co-factor essential for glutathione reductase enzyme activity in trypanosomatids.

Soluble extracts of Trypanosoma brucei, T. cruzi, Leishmania mexicana and Crithidia fasciculata contain a novel enzyme capable of reducing oxidized glutathione by NADPH solely in the presence of an unidentified, dialyzable, heat stable co-factor. Evidence is presented showing that co-factor contains enzymatically reducible thiol group(s), essential for activity. The co-factor is possibly unique to the Kinetoplastida, since dialysate extracts from a wide selection of other organisms would not substitute for trypanosomatid co-factor preparations.

Animals↗
PubMed1984

Preferential effects of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) on pulmonary glutathione reductase and glutathione/glutathione disulfide ratios: possible implications for lung toxicity.

Single doses (8-80 mg/kg) of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) inhibited lung glutathione disulfide (GSSG) reductase in a dose- and time-dependent manner. The loss of enzyme activity persisted up to 8 days after 20 mg of BCNU per kg. A multiple dosing regimen consisting of 5 mg of BCNU per kg/week for 6 weeks decreased lung reductase activity by at least 70%. Recovery was very slow, still remaining well below (68%) control activity for 2 weeks after cessation of BCNU treatment. In contrast, liver GSSG reductase was only slightly decreased by the multi-dose BCNU regimen and rapidly returned to control levels. Pulmonary GSSG concentrations were increased to about 300% of control. This elevation persisted up to 2 weeks after BCNU treatment was completed. There was no effect on total pulmonary glutathione levels during or after BCNU treatment. BCNU administration did not alter hepatic GSSG, although there was a delayed elevation of total liver glutathione. The multi-dose BCNU regimen used in this study leads to the delayed onset of striking pulmonary damage which develops in severity over several weeks after the BCNU treatment is completed. The present results, therefore, suggest that a relatively preferential destruction of lung GSSG reductase by BCNU may precede the development of severe lung toxicity. Considering the probable importance of GSSG reductase in maintaining normal lung homeostasis, this biochemical lesion merits further attention as to its possible role in the pathogenesis of BCNU-induced lung disease.

Animals↗