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Mapping Metabolism: Monitoring Lactate Dehydrogenase Activity Directly in Tissue
Published on: June 21, 2018
Human lactate dehydrogenase A (LDHA) rescues mouse Ldhc-null sperm function.
Huanghui Tang1, Chongwen Duan, Reiner Bleher
1Department of Molecular Biosciences, Northwestern University, Evanston, IL 60208, USA.
Biology of Reproduction
|March 8, 2013
Summary
Spermatozoa need lactate dehydrogenase c (LDHC) for fertility. Introducing human lactate dehydrogenase A (LDHA) into LDHC-deficient mice restored sperm function, suggesting localization is key for male fertility.
Area of Science:
- Reproductive Biology
- Sperm Physiology
- Enzymology
Background:
- Spermatozoa rely on lactate dehydrogenase c (LDHC) for energy metabolism, motility, and fertilization.
- LDHC is crucial for sperm function, but its precise role remains debated.
- LDHC deficiency in mice impairs sperm motility and fertilizing capacity.
Purpose of the Study:
- To investigate the essential characteristics of LDHC for sperm function and fertility.
- To determine if exogenous lactate dehydrogenase A (LDHA) can rescue the phenotype of LDHC-deficient mice.
Main Methods:
- Targeted disruption of the lactate dehydrogenase c (Ldhc) gene in mice.
- Introduction of a human LDHA transgene into Ldhc-null mice.
- Analysis of sperm motility, capacitation, protein tyrosine phosphorylation, and fertilizing capacity.
Main Results:
- Ldhc-null male mice exhibited infertility.
- Transgenic expression of human LDHA in Ldhc-null mice restored sperm motility, capacitation, and fertilizing ability.
- Restored sperm function in rescued mice was not linked to significant changes in lactate or ATP levels.
Conclusions:
- LDHC is essential for male fertility, impacting sperm capacitation, motility, and fertilization.
- Exogenous LDHA can rescue the fertility phenotype in LDHC-deficient mice.
- The cytosolic localization of LDHA, rather than altered metabolic levels, appears responsible for restoring sperm function.
