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Decreased Endogenous Hydrogen Sulfide Generation in Penile Tissues of Diabetic Rats with Erectile Dysfunction.
J Sex Med. 2016 Mar; 13(3):350-60.JS

Abstract

INTRODUCTION

Hydrogen sulfide (H2S) is an endogenous gasotransmitter. The levels of H2S-generating enzyme expression and endogenous H2S production in diabetic rats with erectile dysfunction (ED) remain unknown. The aim of this study was to investigate the expression of the H2S-generating enzymes and endogenous production of H2S in penile tissues of diabetic ED rats.

METHODS

Experimental rats were randomly divided into normal control group, apomorphine (APO)-positive group and APO-negative group. Primary rat corpus cavernosum smooth muscle cells (CCSMCs) and aortic endothelial cells (AECs) were isolated and cultured in vitro under 3 different conditions: normal glucose (NG) condition, high glucose (HG) condition, and osmotic control (OC) condition.

MAIN OUTCOME MEASURES

Erectile function; H2S concentrations in plasma or penile tissues; expression of H2S-generating enzymes and endogenous H2S production in penile tissues, CCSMCs, and AECs.

RESULTS

Erectile function was significantly decreasedin the APO-negative group. In addition to significantly decreased expression of cysteine aminotransferase (CAT), d-amino acid oxidase (DAO), and 3-mercaptopyruvate sulfurtransferase (3-MST), the H2S concentrations in plasma and penile tissues and endogenous H2S production were significantly decreased in the APO-negative group. Endogenous H2S production by cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE) decreased to the same levels in the APO-negative and APO-positive groups as that in the normal control group. However, CBS and CSE expression remained unchanged in the 3 groups. Under HG conditions, H2S-generating enzyme expression in AECs did not change, while CAT, DAO, and 3-MST expression in CCSMCs was significantly decreased. In both cell types, H2S production by these enzymes was decreased in the HG group.

CONCLUSION

Endogenous H2S production was significantly decreased in the diabetic ED rats' penile tissues due to downregulated expression of the CAT/3-MST and DAO/3-MST pathways and low activities of CBS and CSE.

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Authors+Show Affiliations

Zhang Y
Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China; Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Yang J
Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China; Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China. Electronic address: yjun1985win@163.com.
Wang T
Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China; Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Wang SG
Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China; Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Liu JH
Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China; Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Yin CP
Department of Pharmacy, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Ye ZQ
Department of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China; Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

MeSH

AnimalsCystathionine beta-SynthaseCystathionine gamma-LyaseCysteineDiabetes Mellitus, ExperimentalEndothelial CellsErectile DysfunctionHumansHydrogen SulfideMaleNeural PathwaysPenisRatsRats, Sprague-Dawley

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26853047

Citation

Zhang, Yan, et al. "Decreased Endogenous Hydrogen Sulfide Generation in Penile Tissues of Diabetic Rats With Erectile Dysfunction." The Journal of Sexual Medicine, vol. 13, no. 3, 2016, pp. 350-60.
Zhang Y, Yang J, Wang T, et al. Decreased Endogenous Hydrogen Sulfide Generation in Penile Tissues of Diabetic Rats with Erectile Dysfunction. J Sex Med. 2016;13(3):350-60.
Zhang, Y., Yang, J., Wang, T., Wang, S. G., Liu, J. H., Yin, C. P., & Ye, Z. Q. (2016). Decreased Endogenous Hydrogen Sulfide Generation in Penile Tissues of Diabetic Rats with Erectile Dysfunction. The Journal of Sexual Medicine, 13(3), 350-60. https://doi.org/10.1016/j.jsxm.2016.01.002
Zhang Y, et al. Decreased Endogenous Hydrogen Sulfide Generation in Penile Tissues of Diabetic Rats With Erectile Dysfunction. J Sex Med. 2016;13(3):350-60. PubMed PMID: 26853047.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Decreased Endogenous Hydrogen Sulfide Generation in Penile Tissues of Diabetic Rats with Erectile Dysfunction. AU - Zhang,Yan, AU - Yang,Jun, AU - Wang,Tao, AU - Wang,Shao-Gang, AU - Liu,Ji-Hong, AU - Yin,Chun-Ping, AU - Ye,Zhang-Qun, Y1 - 2016/02/04/ PY - 2015/10/02/received PY - 2015/12/04/revised PY - 2016/01/06/accepted PY - 2016/2/9/entrez PY - 2016/2/9/pubmed PY - 2016/9/14/medline KW - Aortic Endothelial Cells KW - Corpus Cavernosum Smooth Muscle Cells KW - Erectile Dysfunction KW - Hydrogen Sulfide KW - Penile Tissues SP - 350 EP - 60 JF - The journal of sexual medicine JO - J Sex Med VL - 13 IS - 3 N2 - INTRODUCTION: Hydrogen sulfide (H2S) is an endogenous gasotransmitter. The levels of H2S-generating enzyme expression and endogenous H2S production in diabetic rats with erectile dysfunction (ED) remain unknown. The aim of this study was to investigate the expression of the H2S-generating enzymes and endogenous production of H2S in penile tissues of diabetic ED rats. METHODS: Experimental rats were randomly divided into normal control group, apomorphine (APO)-positive group and APO-negative group. Primary rat corpus cavernosum smooth muscle cells (CCSMCs) and aortic endothelial cells (AECs) were isolated and cultured in vitro under 3 different conditions: normal glucose (NG) condition, high glucose (HG) condition, and osmotic control (OC) condition. MAIN OUTCOME MEASURES: Erectile function; H2S concentrations in plasma or penile tissues; expression of H2S-generating enzymes and endogenous H2S production in penile tissues, CCSMCs, and AECs. RESULTS: Erectile function was significantly decreasedin the APO-negative group. In addition to significantly decreased expression of cysteine aminotransferase (CAT), d-amino acid oxidase (DAO), and 3-mercaptopyruvate sulfurtransferase (3-MST), the H2S concentrations in plasma and penile tissues and endogenous H2S production were significantly decreased in the APO-negative group. Endogenous H2S production by cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE) decreased to the same levels in the APO-negative and APO-positive groups as that in the normal control group. However, CBS and CSE expression remained unchanged in the 3 groups. Under HG conditions, H2S-generating enzyme expression in AECs did not change, while CAT, DAO, and 3-MST expression in CCSMCs was significantly decreased. In both cell types, H2S production by these enzymes was decreased in the HG group. CONCLUSION: Endogenous H2S production was significantly decreased in the diabetic ED rats' penile tissues due to downregulated expression of the CAT/3-MST and DAO/3-MST pathways and low activities of CBS and CSE. SN - 1743-6109 UR - https://www.unboundmedicine.com/medline/citation/26853047/Decreased_Endogenous_Hydrogen_Sulfide_Generation_in_Penile_Tissues_of_Diabetic_Rats_with_Erectile_Dysfunction_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1743-6095(16)00078-3 DB - PRIME DP - Unbound Medicine ER -