The SYCP3 gene encodes a 236 aminoacid DNA-binding protein. This SYCP3 protein is a structural component of the synaptonemal complex, which mediates the synapsis or homologous pairing of chromosomes during meiosis of the germ cells. As in male mice, null mutation of the Sycp3 gene leads to massive apoptotic cell death in the testis during meiotic prophase, it has been suggested that mutations of human SYCP3 could be associated with non-obstructive azoospermia. Recently, two cases of azoospermic men have been described in which non-obstructive azoospermia was caused by an heterozygous deletion (c.643del) (from a sample of 19 patients diagnosed with azoospermia caused by meiotic arrest). To assess the prevalence of mutations of the SYCP3 gene, we screened the entire coding and flanking intronic sequence of the SYCP3 gene from 36 infertile men with non-obstructive azoospermia by denaturing high-pressure liquid chromatography and direct sequencing. Three novel nucleotide substitutions were identified, one of which was a silent mutation in codon glutamic acid 145 at position 437 (A>G). The two other substitutions were located in introns 2 and 7, a G>T substitution at position +17 and a G>A substitution at position +30, respectively. Moreover, two novel intronic deletions were identified, a 2 bp deletion (gt) at position -133 in intron 1, and a 5 bp deletion (tttta) at position -14 in intron 6. All these intronic sequence variations are polymorphisms rather than disease-causing mutations. Taking account the size of our sample, we conclude that SYCP3 coding sequence point mutations are not an important factor in the aetiology of azoospermia.