Heavy metal exposure, oxidative stress and semen quality: Exploring associations and mediation effects in reproductive-aged men

He, Yinni; Zou, Lijun; Luo, Wenqi; Yi, Zhiyong; Pan, Yang; Yu, Shuyuan; Liu, Ning; Ji, Jiajia; Guo, Yinsheng; Liu, Peiyi; He, Xinpeng; Lv, Ziquan; Huang, Suli

doi:10.1016/j.chemosphere.2019.125498

Cited by 79 publications

(29 citation statements)

References 48 publications

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“…De Franciscis et al investigated fifty healthy men and found that blood Cd concentrations were positively associated with a reduction of sperm motility and teratozoospermia (de Franciscis et al, 2015). He et al measured the urinary levels of oxidative stress markers, semen quality, and urinary levels of three heavy metals including arsenic, Cd and lead in 1020 men and indicate that that higher levels of urinary arsenic, Cd and lead are negatively associated with semen quality and positively associated with increased oxidative stress markers (He et al, 2020).…”

Section: Human Epidemiological Studies Of Cadmiummentioning

confidence: 99%

Toxicological Effects of Cadmium on Mammalian Testis

Zhu

2020

Front. Genet.

102

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Cadmium is a heavy metal, and people are exposed to it through contaminated foods and smoking. In humans and other mammals, cadmium causes damage to male testis. In this review, we summarize the effects of cadmium on the development and function of the testis. Cadmium causes severe structural damage to the seminiferous tubules, Sertoli cells, and blood-testis barrier, thus leading to the loss of sperm. Cadmium hinders Leydig cell development, inhibits Leydig cell function, and induces Leydig cell tumors. Cadmium also disrupts the vascular system of the testis. Cadmium is a reactive oxygen species inducer and possibly induces DNA damage, thus epigenetically regulating somatic cell and germ cell function, leading to male subfertility/infertility.

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Section: Human Epidemiological Studies Of Cadmiummentioning

confidence: 99%

Toxicological Effects of Cadmium on Mammalian Testis

Zhu

2020

Front. Genet.

102

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“…On the other end, mitochondrial DNA (mtDNA) is extremely sensitive to damage from radicals due to the lack of conventional histone proteins and limited mitochondrial damage repair capability; therefore, the resulting accumulation of mtDNA mutations can affect spermatogenetic activity, also causing oligoasthenozoospermia, one of the main causes of male infertility characterized by a reduced number of spermatozoa in the ejaculate and low cell motility, reduced fertilizing capacity and spontaneous abortions in the first months of gestation [ 21 , 22 ]. The 8-Hydroxy-2′-deoxyguanosine (8-OHdG) is known as the early products of oxidative DNA damage [ 23 ] and, for this reason, it has been used as a specific and quantitative biomarker for oxidative stress [ 24 , 25 ]. Indeed, many studies demonstrate the existence of a close correlations between 8-OHdG level and sperm morphology and functionality, thus supporting the potential diagnostic value of this assay in clinical practice [ 26 , 27 ].…”

Section: Introductionmentioning

confidence: 99%

Respiratory Mitochondrial Efficiency and DNA Oxidation in Human Sperm after In Vitro Myo-Inositol Treatment

Governini

Ponchia

Artini

et al. 2020

JCM

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Semen samples are known to contain abnormal amounts of reactive oxygen species (ROS) and oxygen free radicals; therefore, the identification of antioxidant molecules able to counteract the oxidative damage caused by ROS is foresight. Indeed, improving semen quality in terms of motility and reduction in DNA damage, can significantly improve the fertilization potential of sperm in vitro. To this regard, myo-inositol, based on its antioxidant properties, has been reported to be effective in improving sperm quality and motility in oligoasthenozoospermic patients undergoing assisted reproduction techniques when used as a dietary supplementation. Moreover, in vitro treatment demonstrated a direct relationship between myo-inositol, mitochondrial membrane potential and sperm motility. This experimental study aimed to evaluate the effects of myo-inositol (Andrositol-lab) in vitro treatment on sperm motility, capacitation, mitochondrial oxidative phosphorylation and DNA damage. Our results demonstrate that myo-inositol induces a significant increase in sperm motility and in oxygen consumption, the main index of oxidative phosphorylation efficiency and ATP production, both in basal and in in vitro capacitated samples. Moreover, we provide evidence for a significant protective role of myo-inositol against oxidative damage to DNA, thus supporting the in vitro use of myo-inositol in assisted reproductive techniques. Even if further studies are needed to clarify the mechanisms underlying the antioxidant properties of myo-inositol, the present findings significantly extend our knowledge on human male fertility and pave the way to the definition of evidence-based guidelines, aiming to improve the in vitro procedure currently used in ART laboratory for sperm selection.

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“…A clinical fertility study discovered higher Cd content than normal in the seminal plasma and serum of Nigerian male infertility patients, showing that Cd may have a negative influence on fertility of males (Akinloye et al ., 2006). Additionally, various in‐vivo (Ji et al ., 2011; Mouro et al ., 2019) and in‐vitro (Fang et al ., 2020; Wang et al ., 2019) studies using different animal models along with some clinical studies (Buck Louis et al ., 2012; He et al ., 2020) have been performed recently to demonstrate the testicular toxicity of Cd that contributes to the declining fertility of males in the past decade. Therefore, observations from these studies revealed the higher vulnerability of testes to Cd toxicity and warranting the affordable and safer approach towards mitigation of Cd‐induced testicular toxicity.…”

Section: Discussionmentioning

confidence: 99%

Quercetin mediated attenuation of cadmium‐induced oxidative toxicity and apoptosis of spermatogenic cells in caprine testes in vitro

Bhardwaj

Panchal

2021

Environ and Mol Mutagen

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Cadmium (Cd), an environmental toxic heavy metal, has been reported to cause testicular toxicity, which contributes to the recent decline in male fertility worldwide. Quercetin (Qcn), a major dietary antioxidant, has been shown to have protective effects under various pathological conditions. However, whether Qcn provides protection against Cd‐stimulated testicular toxicity remains obscured. The present study was therefore aimed at investigating the ameliorative effect of Qcn supplementation on Cd‐induced toxicity in the goat testis in vitro in a dose‐(10, 50, and 100 μM) and time‐dependent (4 and 8 h) manner. Different cytotoxicity, genotoxicity, and biochemical analyses have been carried out using appropriate methods. Cytotoxicity in testicular cells induced by Cd treatment was apparently mitigated by Qcn treatment, evidenced by decreased apoptotic attributes or frequency in Qcn plus Cd‐treated groups compared to the only Cd‐treated groups. Qcn treatment provides substantial protection to the Cd‐triggered aggression in oxidative (increased MDA levels) and total antioxidant capacity (reduced FRAP activity) in testicular tissue, indicating the anti‐oxidative function of Qcn against Cd exposure. Moreover, Cd‐induced decline in antioxidant status (CAT, SOD, and GST activity) was markedly restored by Qcn supplementation in testicular tissue. In conclusion, this study shows that Qcn treatment significantly attenuated the Cd‐evoked testicular damage, suggesting its beneficial potential in preventing or at least in managing the gonadotoxicity in males induced by steadily increasing Cd contamination in the environment.

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Heavy metal exposure, oxidative stress and semen quality: Exploring associations and mediation effects in reproductive-aged men

Cited by 79 publications

References 48 publications

Toxicological Effects of Cadmium on Mammalian Testis

Toxicological Effects of Cadmium on Mammalian Testis

Respiratory Mitochondrial Efficiency and DNA Oxidation in Human Sperm after In Vitro Myo-Inositol Treatment

Quercetin mediated attenuation of cadmium‐induced oxidative toxicity and apoptosis of spermatogenic cells in caprine testes in vitro

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