Hydrogen peroxide metabolism in alveolar macrophages after exposure to hypoxia and heat

Title:

Hydrogen peroxide metabolism in alveolar macrophages after exposure to hypoxia and heat

Creator:

Lobanova, E.M. and Tahanovich, A.D.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:cd7f4d30-4cf5-45f7-9a17-e58c5d2e8874
uuid:cd7f4d30-4cf5-45f7-9a17-e58c5d2e8874

Subject:

Alveolar macrophages, Hypoxia, Hyperthermia, Hydrogen peroxide, and Free radicals

Type:

article, model:article, and TEXT

Description:

High temperature can change the effects of intra- and intercellular regulators and therefore modify the cellular response to hypoxia. We investigated H2O2 production by alveolar macrophages, isolated from adult male rats, which were incubated under conditions of oxygen deficiency and high temperature (experiment in vitro). The incubation of these cells for 2 hours at 10 % or 5 % oxygen led only to slight fluctuations in the H2O2 level, while the rise of temperature from 37C up to 42C significantly increased its generation. Level of thiobarbituric acid-reactive substances (TBARS) underwent similar changes. Under these conditions the accumulation of H2O2 was found to be caused mainly by its decreased cleavage rather than its enhanced production. This is indicated by decreased catalase and glutathione peroxidase activity together with a parallel absence of significant changes in superoxide dismutase (SOD) activity. Slight fluctuation of reduced glutathione level and the pronounced increase of glucose-6-phosphate dehydrogenase (G6PD) activity were detected. Strong (5 %) but not moderate (10 %) lack of oxygen led to a sharp increase in formation of cellular nitrite ions by alveolar macrophages. In general, our data showed that high temperature did not lead to any qualitative shifts of defined hypoxia-derived changes in oxidant/antioxidant balance in alveolar macrophages, but promoted sensitivity of cells to oxygen shortage.

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2006 Volume:55 | Number:5

Harvested from:

CDK

Metadata only:

false