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Review
. 2022 Mar 23:13:850114.
doi: 10.3389/fgene.2022.850114. eCollection 2022.

Role of Oxidative Stress in Varicocele

Affiliations
Review

Role of Oxidative Stress in Varicocele

Kaixian Wang et al. Front Genet. .

Abstract

According to the official statistics of the World Health Organization, at least 48 million couples and 186 million people suffer from infertility. Varicocele has been recognized as the leading cause of male infertility and can affect spermatogenesis and cause testicular and epididymal disorders through multiple diverse pathophysiological processes. Reactive oxygen species (ROS) produced by oxidative stress have been reconciled as an important pathogenic factor throughout the course of varicocele. Testis respond to heat stress, hypoxia, and inflammation at the cost of producing excessive ROS. High levels of ROS can lead to infertility not only through lipid peroxidation or DNA damage, but also by inactivating enzymes and proteins in spermatogenesis. This review studies the oxidative stress and its role in the pathophysiology and molecular biology of varicocele in the context of a decline in fertility.

Keywords: DNA oxidation damage; antioxidant; infertility; oxidative stress; varicocele.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Abnormal venous valve function. Damaged venous valves result in local venous return, the white arrow represents the direction of blood flow.
FIGURE 2
FIGURE 2
Nutcracker effect. Compression of the superior mesenteric artery on the left renal vein leads to elevated renal vein pressure and spermatic vein return disturbance. The square area represents the superior mesenteric artery pressing against the renal vein.
FIGURE 3
FIGURE 3
DNA oxidative damage. ROS can induce the production of 8-OHDG and the breakage of single stranded DNA and double stranded DNA.
FIGURE 4
FIGURE 4
Oxidative Protein Damage. ROS leads to abnormal protein structure and function.
FIGURE 5
FIGURE 5
Lipid Peroxidation. Lipid peroxidation leads to the change of cell membrane structure and the release of MDA.
FIGURE 6
FIGURE 6
ROS and HSPs. ROS produced by heat stress leads to changes in HSP related and pathways.
FIGURE 7
FIGURE 7
Hypoxia and HIF. Effects of normoxia and hypoxia on HIF- α Different processing results in different functions of HIF and the generation of ROS.
FIGURE 8
FIGURE 8
Inflammation and ROS. ROS induces the activation of NLRP pathway to produce IL-18 and IL-1 β.
FIGURE 9
FIGURE 9
Antioxidants and ROS. Antioxidant function of vitamins C, E and melatonin.

References

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