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Background: Alteration of redox status is a fundamental process in the manifestation of many diseases including malaria. Studies have demonstrated that peptides of the renin-angiotensin-aldosterone system (RAAS), such as Angiotensin Converting Enzyme and Angiotensin II, play a significant role in the pathogenesis of malaria infection by inducing the generation of reactive oxygen species. The present study was aimed at determining the redox status of Plasmodium berghei-infected mice treated with captopril, an angiotensin-converting enzyme inhibitor.
Methodology: Five groups of eight mice each, categorised as control (not infected with P. berghei, not treated), malaria control (P. berghei-infected, not treated), Standard control (P. berghei-infected, treated with 0.03 mg/kg of standard drug, Lonart (Arthemeter 20 mg + Lumefantrine 120 mg), captopril low dose (P. berghei-infected, treated with 0.03 mg/kg captopril) and captopril high dose (P. berghei-infected, treated at with 0.09mg/kg captopril). The mice were treated for 14 days and were sacrificed on the 15th day. Blood samples were collected to determine the levels of reduced glutathione, malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD) and total protein.
Results: Infection with P. berghei significantly (p<0.05) increased MDA, while CAT and SOD levels decreased significantly (p<0.05) compared to mice in the control group. However, MDA levels of mice treated with the standard drug (Artemether 20 mg, Lumefantrine 120 mg), 0.03 and 0.09 mg/kg captopril reduced significantly (p<0.05), while CAT and SOD levels significantly (p<0.05) increased when compared to the malaria control mice. Total protein and reduced glutathione were found to be significantly (p<0.05) high in the malaria control group, whereas a decreased was observed in mice treated with the standard drug and 0.03 mg/kg captopril. Treatment of mice with 0.09 mg/kg captopril significantly increased total protein compared to mice in 0.03 mg/kg captopril group and other groups.
Conclusion: In conclusion, this study has demonstrated that captopril at a low dose can effectively decrease oxidative stress.