Fig. 1

Schematic of the effect of Plasmodium infection and reproductive effort on bird oxidative status. The P (yellow) and R (green) pathways show how Plasmodium infection and reproductive effort, by requiring energy, can lead to an enhancement of superoxide production by the mitochondrial electron transport chain (ETC) during mitochondrial respiration and consumption of oxygen (O₂) to generate adenosine triphosphate (ATP). Oxidants can increase in the red blood cell (RBC) compartment and damage intracellular stages of Plasmodium parasite (merozoite), damage other host’s biomolecules such as lipids of the RBC membrane, enhance plasmatic oxidants and oxidative damage by oxidative reaction chain. The P pathway also shows how Plasmodium infection, by activating the host’s immune system can increase the plasmatic oxidant level. Plasmatic oxidants produced by R and P pathways are able to damage extracellular stages of Plasmodium parasite (merozoite), damage other host’s biomolecules such as lipids of RBC membrane. The plasma antioxidant barrier can counteract the oxidative cascade in the plasma. Reproductive effort can also deplete antioxidant defences and inhibit immune activation. Intracellular stages of Plasmodium can also enhance oxidants in the RBC compartment through haemoglobin degradation. Black paths are not specific to the P or R pathways. Circled numbers indicate oxidative status markers measured in the present study (1 RBC superoxide production, 2 reactive oxygen metabolites in the plasma, 3 RBC membrane resistance to oxidative attack, 4 plasma antioxidant capacity)