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Among them, SLC26A3 acts as a chloride\/bicarbonate exchanger, highly expressed in the gastrointestinal, pancreatic and renal tissues. In humans, mutations in the SLC26A3 gene were shown to induce congenital chloride\u2010losing diarrhea (CLD), a rare autosomal recessive disorder characterized by life\u2010long secretory diarrhea. In view of some reports indicating subfertility in some male CLD patients together with SLC26\u2010A3 and \u2010A6 expression in the male genital tract and sperm cells, we analyzed the male reproductive parameters and functions of SLC26A3 deficient mice, which were previously reported to display CLD gastro\u2010intestinal features. We show that in contrast to Slc26a6, deletion of Slc26a3 is associated with severe lesions and abnormal cytoarchitecture of the epididymis, together with sperm quantitative, morphological and functional defects, which altogether compromised male fertility. 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