A Drosophila model of gestational antimony exposure uncovers growth and developmental disorders caused by disrupting oxidative stress homeostasis

Wang, Xiaoke; Zhou, Peiyao; Zhang, Ziyang; Huang, Qiuru; Chen, Xia; Ji, Li; Cheng, Xinmeng; Shi, Yi; Yu, Shali; Tang, Juan; Sun, Chi; Zhao, Xinyuan; Yu, Jun

doi:10.1016/j.freeradbiomed.2023.09.002

Cited by 9 publications

(10 citation statements)

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“…Previous studies have highlighted the role of oxidative stress in reproductive toxicity induced by metal exposure in Drosophila . Given our observation of the upregulated expression of GstD8 and GstD2 , which encode enzymes associated with GSH metabolism, subsequent in vivo GSH rescue assays were conducted using varying doses of GSH (0.015 and 0.15 mg/mL) in conjunction with TiO 2 NPs (1.8 mg/mL).…”

Section: Resultsmentioning

confidence: 99%

“…Previous studies have highlighted the role of oxidative stress in reproductive toxicity induced by metal exposure in Drosophila . 45 Given our observation of the upregulated expression of GstD8 and GstD2 , which encode enzymes associated with GSH metabolism, subsequent in vivo GSH rescue assays were conducted using varying doses of GSH (0.015 and 0.15 mg/mL) in conjunction with TiO 2 NPs (1.8 mg/mL). Our findings unequivocally demonstrate that GSH supplementation effectively mitigates reproductive toxicity induced by TiO 2 NP exposure, leading to the restoration of the number of Orb-positive spermatid clusters in Drosophila testes ( Figure 6 ).…”

Section: Resultsmentioning

confidence: 99%

“…Besides, puerarin has been shown to reverse oxidative stress and spermatogenesis changes induced by busulfan . Our previous study demonstrated that prenatal exposure to metals, such as antimony (Sb), significantly impaired larval growth and development by disrupting oxidative stress homeostasis . Sb exposure in male testes could also induce reproductive toxicity during spermatogenesis .…”

Section: Discussionmentioning

confidence: 99%

“…Notably, TiO 2 NP exposure has been linked to excessive ROS production in testes, impeding spermatogenesis , Previous studies have shown that exposure to the heavy metal antimony (Sb) in Drosophila led to the upregulation of GstD8 and GstD2 . In our study, an increased expression of GstD8 and GstD2 following TiO 2 NP exposure suggested disrupted oxidative stress homeostasis in Drosophila testes.…”

Section: Discussionmentioning

confidence: 99%

“…Sustaining optimal glutathione levels and its redox equilibrium was imperative for bolstering the structural and functional metamorphoses for spermatid maturation. , Therefore, we employed GSH to rectify the spermatid elongation defects induced by TiO 2 NP exposure by mitigating oxidative stress damage. Evidence suggested that metal exposure-induced oxidative stress imbalance could be mitigated by the antioxidant properties of GSH in Drosophila . Our study further demonstrated that exposure to TiO 2 NPs led to an increase in the LPO levels in Drosophila testes.…”

Section: Discussionmentioning

confidence: 99%

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Exposure to Titanium Dioxide Nanoparticles Leads to Specific Disorders of Spermatid Elongation via Multiple Metabolic Pathways in Drosophila Testes

Cheng,

Jiang,

Huang

et al. 2024

ACS Omega

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Titanium dioxide nanoparticles (TiO 2 NPs) have been extensively utilized in various applications. However, the regulatory mechanism behind the reproductive toxicity induced by TiO 2 NP exposure remains largely elusive. In this study, we employed a Drosophila model to assess potential testicular injuries during spermatogenesis and conducted bulk RNA-Seq analysis to elucidate the underlying mechanisms. Our results reveal that while prolonged exposure to lower concentrations of TiO 2 NPs (0.45 mg/mL) for 30 days did not manifest reproductive toxicity, exposure at concentrations of 0.9 and 1.8 mg/mL significantly impaired spermatid elongation in Drosophila testes. Notably, bulk RNA-seq analysis revealed that TiO 2 NP exposure affected multiple metabolic pathways including carbohydrate metabolism and cytochrome P450. Importantly, the intervention of glutathione (GSH) significantly protected against reproductive toxicity induced by TiO 2 NP exposure, as it restored the number of Orb-positive spermatid clusters in Drosophila testes. Our study provides novel insights into the specific detrimental effects of TiO 2 NP exposure on spermatid elongation through multiple metabolic alterations in Drosophila testes and highlights the protective role of GSH in countering this toxicity.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%