How does G6PD defecient person become malaria resistant?

Glutathione metabolism consists, in large part, of its oxidation to the disulfide and recycling to reduced form by  NADPH by mediation of glutathione reductase . Reduced glutathione is important in the detoxification of free radicals. In normal cells, NADPH is regenerated by G6PD during oxidative stress. Impairment of this step prevents reduced glutathione recycling, exposing  cell to oxidative damage. Alternative pathways to G6PD-dependent NADPH production exist in most human cells bt nt in erythrocytes, and  lack of protein synthetic machinery deprives the erythrocyte of the opportunity to replace enzyme dat has been lost. For these reasons, these cells r uniquely vulnerable to oxidative stress in G6PD deficiency.
If G6PD activity is low, peroxides accumulate, resulting in hemoglobin denaturation and binding to the cell membrane, seen morphologically as Heinz bodies.Hemolysis occurs when erythrocytes pass through the spleen and  Heinz bodies r removed along with a portion of cell membrane. After several passes through spleen,  cell membrane loses competency and  erythrocyte is destroyed.

Now About Malaria Parasites:

Life Cycle of the Malaria Parasite

1. A female Anopheles mosquito carrying malaria-causing parasites feeds on a human and injects the parasites in the form of sporozoites into the bloodstream. The sporozoites travel to the liver and invade liver cells.
2. Over 5-16 days*, the sporozoites grow, divide, and produce tens of thousands of haploid forms, called merozoites, per liver cell. Some malaria parasite species also produce hypnozoites in the liver that remain dormant for extended periods, causing relapses weeks or months later.
3. The merozoites exit the liver cells and re-enter the bloodstream, beginning a cycle of invasion of red blood cells, known as asexual replication. In the red blood cells they develop into mature schizonts, which rupture, releasing newly formed merozoites that then reinvade other red blood cells. This cycle of invasion and cell rupture repeats every 1-3 days* and can result in thousands of parasite-infected red blood cells in the host bloodstream, leading to illness and complications of malaria that can last for months if not treated.
4. Some of the merozoite-infected blood cells leave the cycle of asexual replication. Instead of replicating, the merozoites in these cells develop into sexual forms of the parasite, called male and female gametocytes. In some malaria species, young gametocytes sequester in the bone marrow and some organs while late stage (stage V) gametocytes, circulate in the bloodstream.
5. When a mosquito bites an infected human, it ingests the gametocytes. In the mosquito midgut, the infected human red blood cells burst, releasing the gametocytes, which develop further into mature sexual forms called gametes. Male and female gametes fuse to form diploid zygotes, which develop into actively moving ookinetes that burrow through the mosquito midgut wall and form oocysts on the other side.
6. Growth and division of each oocyst produces thousands of active haploid forms called sporozoites. After 8-15 days*, the oocyst bursts, releasing sporozoites into the body cavity of the mosquito, from which they travel to and invade the mosquito salivary glands. The cycle of human infection re-starts when the mosquito takes a blood meal, injecting the sporozoites from its salivary glands into the human bloodstream

Now as malaria parasites are dependent on RBC for replication and in G6PD defeciency RBC are hemolysed so Parasites can not divide and grow and the person in resistant to malaria.