Abstract：
OBJECTIVE: Plastic particles (PP) pollution is a global environmental concern. Although the reproductive toxicity of PP is primarily understood for invertebrates, the evidence for mammals is still fragmented. We used a systematic review framework to investigate the reproductive impact of microplastics and nanoplastics (MNP) on mammals.
METHODS: Research records were screened from Embase, Medline, Scopus and Web of Science. Twelve original papers were identified and reviewed. Immunological, oxidative and morphofunctional outcomes, and the risk of bias in all studies reviewed were analyzed.
RESULTS: These studies indicated that PP can accumulate in the gonads, triggering seminiferous degeneration, Sertoli cells death, blood-testis barrier disruption, sperm degeneration, malformation, reduced number and mobility, ovarian cysts, reduced follicular growth and granulosa cells death. Gonadal damage was associated with upregulation of prooxidant mediators (oxygen reactive species, lipid and DNA oxidation), cell death, proinflammatory molecular pathways and cytokines, as well as inhibition of enzymatic and non-enzymatic antioxidant defense mechanisms. Spermatogenesis, folliculogenesis, testosterone, progesterone and estrogen levels were also impaired in PP-treated animals, which were potentially associated with down-regulation of molecules involved in germ cells microstructural organization (occludin, N-cadherin, β-catenin and connexin 43) and steroidogenesis, such as hydroxysteroid dehydrogenases, steroidogenic acute regulatory proteins, follicle stimulating and luteinizing hormones. Selection, performance and detection bias were the main limitations identified.
CONCLUSIONS: Current evidence indicates that PP can induce dose-dependent microstructural and functional gonadal damage, which is orchestrated by pro-oxidant and pro-inflammatory mechanisms that disrupt genes, molecular effectors, and hormones that control spermatogenesis and folliculogenesis.
METHODS: Research records were screened from Embase, Medline, Scopus and Web of Science. Twelve original papers were identified and reviewed. Immunological, oxidative and morphofunctional outcomes, and the risk of bias in all studies reviewed were analyzed.
RESULTS: These studies indicated that PP can accumulate in the gonads, triggering seminiferous degeneration, Sertoli cells death, blood-testis barrier disruption, sperm degeneration, malformation, reduced number and mobility, ovarian cysts, reduced follicular growth and granulosa cells death. Gonadal damage was associated with upregulation of prooxidant mediators (oxygen reactive species, lipid and DNA oxidation), cell death, proinflammatory molecular pathways and cytokines, as well as inhibition of enzymatic and non-enzymatic antioxidant defense mechanisms. Spermatogenesis, folliculogenesis, testosterone, progesterone and estrogen levels were also impaired in PP-treated animals, which were potentially associated with down-regulation of molecules involved in germ cells microstructural organization (occludin, N-cadherin, β-catenin and connexin 43) and steroidogenesis, such as hydroxysteroid dehydrogenases, steroidogenic acute regulatory proteins, follicle stimulating and luteinizing hormones. Selection, performance and detection bias were the main limitations identified.
CONCLUSIONS: Current evidence indicates that PP can induce dose-dependent microstructural and functional gonadal damage, which is orchestrated by pro-oxidant and pro-inflammatory mechanisms that disrupt genes, molecular effectors, and hormones that control spermatogenesis and folliculogenesis.
摘要：
目的：塑料颗粒（PP）污染是全球环境问题。虽然PP的生殖毒性主要被理解为无脊椎动物，哺乳动物的证据仍然支离破碎。我们使用系统综述框架来研究微塑料和纳米塑料（MNP）对哺乳动物的生殖影响。
方法：从Embase筛选研究记录，Medline,Scopus和WebofScience确定并审查了12篇原始论文。免疫学,氧化和形态功能结果，并分析了所有综述研究的偏倚风险.
结果：这些研究表明PP可以在性腺中积累，引发生精变性，支持细胞死亡，血-睾丸屏障破坏,精子变性,畸形,减少数量和流动性，卵巢囊肿,减少卵泡生长和颗粒细胞死亡。性腺损伤与促氧化剂介质的上调有关（氧反应性物质，脂质和DNA氧化），细胞死亡,促炎分子途径和细胞因子，以及抑制酶和非酶抗氧化防御机制。精子发生,卵泡发生，睾丸激素，在PP治疗的动物中，孕激素和雌激素水平也受损，这可能与生殖细胞微结构组织中涉及的分子的下调相关(occludin，N-钙黏着蛋白,β-连环蛋白和连接蛋白43)和类固醇生成，如羟基类固醇脱氢酶，类固醇生成急性调节蛋白，促卵泡和促黄体激素。选择,性能和检测偏差是确定的主要限制。
结论：目前的证据表明，PP可以诱导剂量依赖性的微观结构和功能性腺损伤，这是由破坏基因的促氧化和促炎机制精心策划的，分子效应子，和控制精子生成和卵泡生成的激素。
方法：从Embase筛选研究记录，Medline,Scopus和WebofScience确定并审查了12篇原始论文。免疫学,氧化和形态功能结果，并分析了所有综述研究的偏倚风险.
结果：这些研究表明PP可以在性腺中积累，引发生精变性，支持细胞死亡，血-睾丸屏障破坏,精子变性,畸形,减少数量和流动性，卵巢囊肿,减少卵泡生长和颗粒细胞死亡。性腺损伤与促氧化剂介质的上调有关（氧反应性物质，脂质和DNA氧化），细胞死亡,促炎分子途径和细胞因子，以及抑制酶和非酶抗氧化防御机制。精子发生,卵泡发生，睾丸激素，在PP治疗的动物中，孕激素和雌激素水平也受损，这可能与生殖细胞微结构组织中涉及的分子的下调相关(occludin，N-钙黏着蛋白,β-连环蛋白和连接蛋白43)和类固醇生成，如羟基类固醇脱氢酶，类固醇生成急性调节蛋白，促卵泡和促黄体激素。选择,性能和检测偏差是确定的主要限制。
结论：目前的证据表明，PP可以诱导剂量依赖性的微观结构和功能性腺损伤，这是由破坏基因的促氧化和促炎机制精心策划的，分子效应子，和控制精子生成和卵泡生成的激素。
