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Oxidative stress and protective mechanisms in erythrocytes in relation to Plasmodium vinckei load
Abstract:
The protection of mouse erythrocytes (RBC) parasitized with Plasmodium vinckei vinckei against activated oxygen species was examined in relation to the intraerythrocytic parasite load. RBC from highly infected animals were separated by density gradient centrifugation into six bands with increasing parasite content and with parasitemias ranging from 17% to 100%. Increase in parasite load was accompanied by a decrease in the activities of the enzymes superoxide dismutase (EC 1.15.1.1), catalase (EC 1.11.1.6), glutathione peroxidase (EC 1.11.1.9), glutathione reductase [NAD(P)H] (EC 1.6.4.2), and NADH-methemoglobin reductase (EC 1.6.2.2; NADH:ferricytochrome b5 oxidoreductase) in the RBC lysates. In contrast, the total amount of reduced glutathione increased in the highly parasitized bands. Furthermore, the vitamin E content of all RBC bands, including the one that contained mainly nonparasitized erythrocytes, was 3- to 5-fold higher than that of control noninfected RBC. Increasing parasite load was accompanied by an increase in the production of malonyldialdehyde, indicating enhanced lipid peroxidation. Our results indicate that oxidative stress is experienced by all RBC during a malarial infection and is accompanied by a variety of changes in the antioxidant defense mechanisms of the host and the parasite. Furthermore, it appears that the plasma membrane of the host cell is better protected against oxidative injury than are the membranes surrounding the parasite.
Insights
Malaria infection causes oxidative stress in mouse red blood cells (RBC). As parasite load increases, antioxidant enzyme activity decreases, but vitamin E levels rise, suggesting complex host-parasite antioxidant defenses.
Area of Science:
- Biochemistry
- Parasitology
- Cell Biology
Background:
- Malaria, caused by Plasmodium parasites, significantly impacts red blood cells (RBCs).
- Oxidative stress is implicated in malaria pathogenesis, but its relationship with parasite load is not fully understood.
Purpose of the Study:
- To investigate the impact of Plasmodium vinckei vinckei parasite load on mouse erythrocyte antioxidant defense mechanisms.
- To assess the levels of specific antioxidant enzymes, glutathione, vitamin E, and lipid peroxidation markers in relation to parasitemia.
Main Methods:
- Density gradient centrifugation was used to separate infected mouse RBCs into fractions with varying parasite loads (17%–100% parasitemia).
- Enzyme activities (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, NADH-methemoglobin reductase), reduced glutathione, vitamin E content, and malonyldialdehyde production were measured.
Main Results:
- Increasing parasite load correlated with decreased activities of key antioxidant enzymes.
- Total reduced glutathione and vitamin E levels increased with higher parasite loads, even in non-parasitized RBCs.
- Malondialdehyde production increased, indicating enhanced lipid peroxidation in infected RBCs.
Conclusions:
- Malaria infection induces oxidative stress in all mouse RBCs, altering host and parasite antioxidant defenses.
- Host erythrocyte plasma membranes show greater protection against oxidative injury compared to parasite membranes.