Cytotoxic mechanism related to dihydrolipoamide dehydrogenase in Leydig cells exposed to heavy metals

Ji, Xunmin; Li, Zhiliang; Chen, Hongxia; Li, Junqi; Tian, Huajian; Li, Zengli; Gao, Xuejuan; Xiang, Qi; Su, Zhijian; Huang, Yadong; Zhang, Qihao

doi:10.1016/j.tox.2015.05.003

Cited by 25 publications

(16 citation statements)

References 49 publications

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“…61,62 In particular, two previous studies 26,27 using exposure protocols based on daily administration of the NPs for 35 days have established that ZnO NPs have cytotoxic actions on testicular germ cells in a dose-dependent manner. In line with these studies, we found that a single systemic injection of ZnO NPs caused alteration in the structure of seminiferous epithelium and the production of morphologically abnormal spermatozoa.…”

Section: Zno Nps Induce Nuclear Dna Leakage and Breakagementioning

confidence: 99%

“…[63][64][65][66] Heavy metals are also common environmental toxicants that adversely affect steroid biosynthesis, causing irreversible degeneration or atrophy of the seminiferous tubules, testicular injury, and sex hormone disturbances. 26,27,67 Since the development and use of engineered NPs, many studies have examined their adverse effects on the mouse testes. Serious concerns have been expressed about the potential risks of engineered NPs, and various functional and pathological disorders and reduced sperm counts have been observed, together with the suppression of spermatogenesis, marked changes in testicular enzymes, and oxidative stress in the testes.…”

Section: Zno Nps Induce Nuclear Dna Leakage and Breakagementioning

confidence: 99%

“…[23][24][25] Concerning the effect of ZnO NP on male reproduction, it has been reported that these NPs can act as a testicular toxicant. [26][27][28] Ji et al have reported that LCs exposed to 10/20 μM of cadmium (Cd) had reduced levels of steroid hormone due to inhibition of activation of cyclic adenosine monophosphate/protein kinase A, protein kinase C signaling pathway, and the steroidogenic enzymes StAR, CYP11A1, and 3β-HSD. 26 Also, Talebi et al reported that epithelial vacuolization, sloughing of germ cells, and detachment of mice were significantly increased after treatment with ZnO NPs, and also, ZnO NPs caused a significant decrease in seminiferous tubule diameter, seminiferous epithelium height, and maturation arrest.…”

Section: Introductionmentioning

confidence: 99%

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Cytotoxic effects of ZnO nanoparticles on mouse testicular cells

Han¹,

Yan²,

Ge³

et al. 2016

IJN

102

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Nanoscience and nanotechnology are developing rapidly, and the applications of nanoparticles (NPs) have been found in several fields. At present, NPs are widely used in traditional consumer and industrial products, however, the properties and safety of NPs are still unclear and there are concerns about their potential environmental and health effects. The aim of the present study was to investigate the potential toxicity of ZnO NPs on testicular cells using both in vitro and in vivo systems in a mouse experimental model

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Section: Zno Nps Induce Nuclear Dna Leakage and Breakagementioning

confidence: 99%

Section: Zno Nps Induce Nuclear Dna Leakage and Breakagementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Cytotoxic effects of ZnO nanoparticles on mouse testicular cells

Han¹,

Yan²,

Ge³

et al. 2016

IJN

102

View full text Add to dashboard Cite

show abstract

“…Previous studies demonstrated that Cd increases the expression of MAPK pERK 1/2 (Ji et al, 2015; Minutoli et al, 2015b), which was considered one of the downstream signal transducers involved in the disassembly of focal adhesion-like ectoplasmic specialization structures in the adluminal compartment of seminiferous tubules (Wong and Cheng, 2005). Furthermore, it is known that other MAPK family components (p38 and JNK) are also able to regulate BTB through TGF-β3 (Lui et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Polydeoxyribonucleotide, an Adenosine-A2A Receptor Agonist, Preserves Blood Testis Barrier from Cadmium-Induced Injury

et al. 2017

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Cadmium (Cd) impairs blood-testis barrier (BTB). Polydeoxyribonucleotide (PDRN), an adenosine A2A agonist, has positive effects on male reproductive system. We investigated the effects of PDRN on the morphological and functional changes induced by Cd in mice testes. Adult Swiss mice were divided into four groups: controls administered with 0.9% NaCl (1 ml/kg, i.p., daily) or with PDRN (8 mg/kg, i.p. daily), animals challenged with Cd chloride (CdCl2; 2 mg/kg, i.p, daily) and animals challenged with CdCl2 (2 mg/kg, i.p., daily) and treated with PDRN (8 mg/kg, i.p., daily). Experiments lasted 14 days. Testes were processed for biochemical, structural, and ultrastructural evaluation and hormones were assayed in serum. CdCl2 increased pERK 1/2 expression and Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH) levels; it decreased testosterone (TE) and inhibin-B levels and induced structural damages in extratubular compartment and in seminiferous epithelium, with ultrastructural features of BTB disruption. Many TUNEL-positive germ cells were present. CdCl2 increased tubular TGF-β3 immunoreactivity and reduced claudin-11, occludin, and N-cadherin immunoreactivity. PDRN administration reduced pERK 1/2 expression, FSH, and LH levels; it increased TE and inhibin-B levels, ameliorated germinal epithelium changes and protected BTB ultrastructure. Few TUNEL-positive germ cells were present and the extratubular compartment was preserved. Furthermore, PDRN decreased TGF-β3 immunoreactivity and enhanced claudin-11, occludin, and N-cadherin immunoreactivity. We demonstrate a protective effect of PDRN on Cd-induced damages of BTB and suggest that PDRN may play an important role against Cd, particularly against its harmful effects on gametogenesis.

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“…Mouse models have demonstrated Cd exposure may down-regulate the expression of CYP11A1 (Hu et al, 2014). Similarly, the expression of CYP11A1 and HSD3B1 have been shown to be down-regulated in response to Cd in Leydig Cells (Ji et al, 2015) and in cultured trophoblasts (Kawai et al, 2002). Whereas, Wang et al (2014) observed increased corticosterone synthesis and significantly up-regulated CYP11A1 (and increased HSD3B1 though not statistically significant) in placenta of rats exposed to Cd during pregnancy, and that increased circulating corticosterone was associated with PE-like symptoms and IUGR (Wang et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Maternal exposure to selenium and cadmium, fetal growth, and placental expression of steroidogenic and apoptotic genes

Everson

Kappil

Hao

et al. 2017

Environmental Research

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Background Cadmium (Cd) and selenium (Se) antagonistically influence redox balance and apoptotic signaling, with Cd potentially promoting and Se inhibiting oxidative stress and apoptosis. Alterations to placental redox and apoptotic functions by maternal exposure to Cd and Se during pregnancy may explain some of the Cd and Se associations with fetal development. Objectives Investigate associations between Cd and Se concentrations in maternal toenails with placental expression patterns of tumor necrosis factor (TNF) and steroidogenic genes involved in redox reactions and test associations with fetal growth. Methods In a sub-sample from the Rhode Island Child Health Study (n = 173), we investigated the relationships between: (1) maternal toenail Cd and Se concentrations and fetal growth using logistic regression, (2) Cd and Se interactions with factor scores from placental TNF and steroidogenic expression patterns (RNAseq) using linear models, and (3) TNF and steroidogenic expression factors with fetal growth via analysis of covariance. Results Se was associated with decreased odds of intrauterine growth restriction (IUGR) (OR = 0.27, p-value = 0.045). Cd was associated with increased odds of IUGR (OR = 1.95, p-value = 0.13) and small for gestational age (SGA) births (OR = 1.46, p-value = 0.11), though not statistically significant. Cd and Se concentrations were antagonistically associated with placental TNF and steroidogenic expression patterns, which also differed by birth size. Conclusions Se may act as an antagonist to Cd and as a modifiable protective factor in fetal growth restriction, and these data suggest these effects may be due to associated variations in the regulation of genes involved in placental redox balance and/or apoptotic signaling.

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Cytotoxic mechanism related to dihydrolipoamide dehydrogenase in Leydig cells exposed to heavy metals

Cited by 25 publications

References 49 publications

Cytotoxic effects of ZnO nanoparticles on mouse testicular cells

Cytotoxic effects of ZnO nanoparticles on mouse testicular cells

Polydeoxyribonucleotide, an Adenosine-A2A Receptor Agonist, Preserves Blood Testis Barrier from Cadmium-Induced Injury

Maternal exposure to selenium and cadmium, fetal growth, and placental expression of steroidogenic and apoptotic genes

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