Potential Benefits of Lycopene Consumption: Rationale for Using It as an Adjuvant Treatment for Malaria Patients and in Several Diseases

Abstract

Malaria is a disease that affects thousands of people around the world every year. Its pathogenesis is associated with the production of reactive oxygen and nitrogen species (RONS) and lower levels of micronutrients and antioxidants. Patients under drug treatment have high levels of oxidative stress biomarkers in the body tissues, which limits the use of these drugs. Therefore, several studies have suggested that RONS inhibition may represent an adjuvant therapeutic strategy in the treatment of these patients by increasing the antioxidant capacity of the host. In this sense, supplementation with antioxidant compounds such as zinc, selenium, and vitamins A, C, and E has been suggested as part of the treatment. Among dietary antioxidants, lycopene is the most powerful antioxidant among the main carotenoids. This review aimed to describe the main mechanisms inducing oxidative stress during malaria, highlighting the production of RONS as a defense mechanism against the infection induced by the ischemia-reperfusion syndrome, the metabolism of the parasite, and the metabolism of antimalarial drugs. Furthermore, the effects of lycopene on several diseases in which oxidative stress is implicated as a cause are outlined, providing information about its mechanism of action, and providing an evidence-based justification for its supplementation in malaria.

Keywords: adjuvant treatment; antioxidants; carotenoids; lycopene; malaria; oxidative stress; supplementation.

Figure 1

Production of reactive oxygen species from the transfer of electrons from the electron transport chain.

Figure 2

Oxidative stress as a host defense mechanism in response to infection by Plasmodium sp.

Figure 3

Oxidative stress due to ischemia-reperfusion syndrome during malaria.

Figure 4

Oxidative stress as a consequence of parasite metabolism.

Figure 5

Consequences of the multiplication of parasites in the erythrocyte.

Figure 6

All-trans-lycopene and cis-lycopene structures.

Figure 7

Anti-inflammatory effects of lycopene. (A) Direct anti-inflammatory activity. (B) Indirect anti-inflammatory activity. TGF-β, Transforming growth factor-beta; AP-1, activator protein-1; JNK, c-jun N-terminal kinase; MAPK, mitogen-activated protein kinases; I-κB, kappa B inhibitory protein; LPS, lipopolysaccharide; TNF-α, tumor necrosis factor-alpha; IL-1, interleukin 1; IL-6, interleukin 6; MCP-1, monocyte chemoattractant protein 1.

Figure 8

Antioxidant effect of lycopene. (A) Direct antioxidant activity. (B) Indirect antioxidant activity. Keap1, Kelch-like inhibitory protein 1; Nrf2, erythroid nuclear factor 2; GSH, glutathione; SOD, superoxide dismutase; CAT, catalase; GSH-Px, glutathione peroxidase; PI3K/AKT, phosphoinositide 3-kinase/AKT.