Negative effects of ROS generated during linear sperm motility on gene expression and ATP generation in boar sperm mitochondria.


Journal

Free radical biology & medicine
ISSN: 1873-4596
Titre abrégé: Free Radic Biol Med
Pays: United States
ID NLM: 8709159

Informations de publication

Date de publication:
09 2019
Historique:
received: 03 04 2019
revised: 06 06 2019
accepted: 14 06 2019
pubmed: 19 6 2019
medline: 14 7 2020
entrez: 19 6 2019
Statut: ppublish

Résumé

Mitochondrial oxidative phosphorylation (OXPHOS) is essential for ATP production to maintain sperm linear motility during migration from the uterus to the oviduct. However, ROS are generated as by-products of OXPHOS, causing stress and damaging the sperm quality. This study aimed to clarify the ROS targets in sperm mitochondria that decrease linear motility and to investigate whether mitochondria-target antioxidants (PQQ and CoQ10) affect mitochondrial activity and sperm motility. Sperm linear motility pattern, ATP production, and mitochondrial activity were decreased with increasing ROS levels during incubation in the low-glucose medium. However, sperm motility patterns and ROS levels were not significantly changed in the high-glucose medium. Moreover, the gene expression system (mt-DNA, mitochondrial transcription factor-A (TFAM) and RNA polymerase (POLRMT)) in sperm mitochondria was damaged during incubation in the low-glucose medium. Interestingly, PQQ treatment increased the mt-DNA stability and decreased the damage to TFAM and POLRMT, which resulted in high expression of mitochondrial genes. Furthermore, the antioxidants increased mitochondrial activity and maintained sperm linear motility under the low glucose condition. These results revealed that both ATP production and the mitochondrial transcription system are damaged with increasing ROS levels in sperm that show a linear motility pattern. Treatment with antioxidants, such as PQQ and CoQ10, is beneficial tool to maintain sperm linear motility.

Identifiants

pubmed: 31212063
pii: S0891-5849(19)30566-0
doi: 10.1016/j.freeradbiomed.2019.06.018
pii:
doi:

Substances chimiques

Antioxidants 0
Culture Media 0
DNA, Mitochondrial 0
Reactive Oxygen Species 0
Ubiquinone 1339-63-5
PQQ Cofactor 72909-34-3
Adenosine Triphosphate 8L70Q75FXE
coenzyme Q10 EJ27X76M46
Glucose IY9XDZ35W2

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

159-171

Informations de copyright

Copyright © 2019 Elsevier Inc. All rights reserved.

Auteurs

Zhendong Zhu (Z)

Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Shaanxi, China; Laboratory of Reproductive Endocrinology, Graduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima, Japan.

Tomoko Kawai (T)

Laboratory of Reproductive Endocrinology, Graduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima, Japan.

Takashi Umehara (T)

Laboratory of Reproductive Endocrinology, Graduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima, Japan.

S A Masudul Hoque (SAM)

Laboratory of Reproductive Endocrinology, Graduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima, Japan; Bangabandhu Sheikh Mujibur Rahman Agricultural University, Gazipur, 1706, Bangladesh.

Wenxian Zeng (W)

Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Shaanxi, China. Electronic address: zengwenxian2013@126.com.

Masayuki Shimada (M)

Laboratory of Reproductive Endocrinology, Graduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima, Japan. Electronic address: mashimad@hiroshima-u.ac.jp.

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Classifications MeSH