Interrelationships Between Apoptosis and Fertility in Bull
Sperm |
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Authors: | Sule DOGAN Melissa C MASON Aruna GOVINDARAJU Lauren BELSER Abdullah KAYA John STOKES Dennis ROWE Erdogan MEMILI |
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Institution: | 1)Department of Animal and Dairy Sciences, Mississippi State University, Starkville, MS 39762, USA;2)Alcorn State University, Lorman, MS 39096, USA;3)Alta Genetics, Incorporated, Watertown, WI 53094, USA;4)Department of Basic Sciences, Mississippi State University, Starkville, MS 39762, USA;5)Mississippi Agricultural and Forestry Experiment Station, Mississippi State University, Starkville, MS 39762, USA |
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Abstract: | Male fertility, the ability of sperm to fertilize and activate the egg and support early
embryogenesis, is vital for mammalian reproduction. Despite producing adequate numbers of
sperm with normal motility and morphology, some males suffer from low fertility whose
molecular mechanisms are not known. The objective was to determine apoptosis in sperm from
high and low fertility bulls and its relationship with male fertility. DNA damage,
phosphatidylserine (PS) translocation, and expression of pro- and anti-apoptotic proteins
(BAX and BCL-2) in the sperm were determined using TUNEL, Annexin V, and immunoblotting
approaches, respectively. Amounts of apoptotic spermatozoa were 2.86 (± 1.31) and 3.00 (±
0.96) in high and low fertility bulls, respectively (P=0.548), and were not correlated
with fertility. There was a negative correlation between early necrotic spermatozoa and
viable spermatozoa (r = –0.99, P<0.0001). Fertility scores were correlated with live
spermatozoa detected by eosin-nigrosin test and necrotic spermatozoa determined via flow
cytometry (r = –0.49, P<0.006 and r = –0.266, P<0.0113, respectively). BAX level was
higher in low fertile group than high fertile group; however, this difference was not
statistically significant due to the variations of bull samples (Bull 1–3
vs. Bull 4–5) in low fertile group (P<0.283). BCL-2 was not
detectable in any of the sperm samples. The results shed light onto molecular and cellular
underpinnings of male fertility. |
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Keywords: | Apoptosis DNA damage Male infertility Sperm |
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