Journal of Human Reproductive Science
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ORIGINAL ARTICLE Table of Contents   
Year : 2016  |  Volume : 9  |  Issue : 1  |  Page : 35-40
Association of large scale 4977-bp "common" deletions in sperm mitochondrial DNA with asthenozoospermia and oligoasthenoteratozoospermia

1 Department of Anatomy, Human Genetic Division, Mahatma Gandhi Institute of Medical Sciences, Wardha, Maharashtra, India
2 Department of Physiology, Mahatma Gandhi Institute of Medical Sciences, Wardha, Maharashtra, India

Correspondence Address:
Dr. Asoke K Pal
Department of Anatomy, Human Genetic Division, Mahatma Gandhi Institute of Medical Sciences, Sevagram, Wardha - 442102, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0974-1208.178635

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OBJECTIVE: To determine the association of large-scale mitochondrial DNA (mtDNA) deletions with abnormal sperm or abnormal flagellar movement of human spermatozoa in asthenozoospermia and oligoasthenoteratozoospermia (OAT) subjects using percoll gradients fractionation and long-range polymerase chain reaction (PCR). DESIGN: We investigated sixty infertile men and thirty normal healthy fertile controls. Of sixty infertile men, 39 were asthenozoospermia and 21 were OAT. MATERIALS AND METHODS: Percoll gradients discontinuous technique was used for separation of spermatozoa on the basis of their motility. Long-range PCR was used for detection of “common ” 4977-bp deletions, and primer shift technique was used for confirmation of deletions. RESULTS: Overall fourteen subjects (14/60; 23.3%) of which eight (8/39; 20.5%) asthenozoospermia and six (6/21; 28.6%) OAT had shown deletions of 4977-bp. Deletions were more common (23.3%) in 40% fraction than 60% (11.6%) and 80% (5%) fractions. Sequencing results had shown deleted region of mtDNA. CONCLUSION: Abnormal spermatozoa had more number of mtDNA deletions than normal sperm, and abnormal spermatozoa had lost genes for the oxidative phosphorylation. Our findings suggest that large-scale 4977-bp mtDNA deletions in the spermatozoa from the infertile subjects cause the asthenozoospermic and OAT pathophysiological conditions in infertile males.

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