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Modulation of arachidonic acid turnover in macrophages by cadmium
D C Ramirez1, C M Riera, M S Gimenez
1Department of Biochemistry and Biological Sciences, Faculty of Chemistry, Biochemistry and Pharmacy, National University of San Luis, Avenida Ejercito de los Andes 950, 5700 San Luis, Argentina. dramirez@unsl.edu.ar
Abstract:
The effects of cadmium (Cd) induced redox changes on arachidonic acid (AA) turnover in mouse resident peritoneal macrophages (pM) were studied. The pre-incubation of pM in a medium containing glutathione (GSH, 0.1 or 1 mM) for 6 h protects pM from loss of viability and AA uptake diminution induced by Cd with regard to non pre-incubated cultures. The exposure of macrophages to Cd 10 microM decreases AA uptake within 2 h and increases AA release in relation to non-exposed macrophages. It also enhances AA mobilization and reactive oxygen species (ROS) release induced by okadaic acid and opsonized zimosan and decreases those induced by lipopolysaccharide, but does not modify either AA mobilization or ROS release induced by phorbol ester. These results might suggest that redox changes induced by Cd produce an important impact on AA turnover in macrophages; information that is relevant in the understanding of the cellular toxicity of this metal.
Insights
Cadmium exposure impacts macrophage arachidonic acid turnover and viability. Glutathione pre-incubation protects against these cadmium-induced effects, offering insights into metal toxicity.
Area of Science:
- Toxicology
- Cell Biology
- Biochemistry
Background:
- Cadmium (Cd) is a toxic metal.
- Redox changes are implicated in cellular toxicity.
- Arachidonic acid (AA) turnover is crucial in macrophage function.
Purpose of the Study:
- To investigate the effects of cadmium-induced redox changes on arachidonic acid turnover in mouse resident peritoneal macrophages (pM).
- To assess the protective role of glutathione (GSH) against cadmium toxicity in macrophages.
Main Methods:
- Mouse resident peritoneal macrophages were exposed to cadmium (Cd) and/or glutathione (GSH).
- Arachidonic acid (AA) uptake and release were measured.
- Reactive oxygen species (ROS) release was assessed following various stimuli.
- Macrophage viability was evaluated.
Main Results:
- Cadmium exposure decreased macrophage viability and AA uptake.
- Glutathione pre-incubation protected macrophages from Cd-induced toxicity.
- Cadmium altered AA mobilization and ROS release in response to different stimuli, suggesting a role for redox changes.
- Specific signaling pathways (okadaic acid, zimosan, LPS, phorbol ester) were differentially affected.
Conclusions:
- Cadmium-induced redox changes significantly impact macrophage arachidonic acid turnover.
- Glutathione offers protection against cadmium toxicity in macrophages.
- Understanding these mechanisms is vital for comprehending cadmium's cellular toxicity.