From Wikipedia...
Oculocutaneous albinism is generally the result of the biological inheritance of genetically recessive alleles (genes) passed from both parents of an individual for example OCA1 (a gene on chromosome 11) and OCA2 (a gene on chromosome 15).
A mutation in the human TRP-1 gene (on chromosome 9) may result in the deregulation of melanocyte tyrosinase enzymes, a change that is hypothesized to promote brown versus black melanin synthesis, resulting in a third oculocutaneous albinism (OCA) genotype, ″OCA3″.[12] Some rare forms are inherited from only one parent. There are other genetic mutations which are proven to be associated with albinism. All alterations, however, lead to changes in melanin production in the body.[8][13] Some of these are associated with increased risk of skin cancer (see list of such genetic variations).
The chance of offspring with albinism resulting from the pairing of an organism with albinism and one without albinism is low. However, because organisms (including humans) can be carriers of genes for albinism without exhibiting any traits, albinistic offspring can be produced by two non-albinistic parents. Albinism usually occurs with equal frequency in both sexes.[8] An exception to this is ocular albinism, which it is passed on to offspring through X-linked inheritance. Thus, ocular albinism occurs more frequently in males as they have a single X and Y chromosome, unlike females, whose genetics are characterized by two X chromosomes.[14]
There are two different forms of albinism: a partial lack of the melanin is known as hypomelanism, or hypomelanosis, and the total absence of melanin is known as amelanism or amelanosis.
The enzyme defect responsible for OCA1-type albinism is tyrosine 3-monooxygenase (tyrosinase), which synthesizes melanin from the amino acid tyrosine.