| Objective:Microplastics(MPs)are ubiquitous in the world and their impact on human health has attracted increasing attention.Polystyrene microplastics(PS-MPs),one of the most common microplastics,have been widely detected in the environment.It has been shown that PS-MPs have toxic effects on multiple systems in the body.In this study,mice were exposed to polystyrene nanoparticles(PS-NPs)at different concentrations through drinking water during pregnancy and lactation to observe their trans-generational toxicities.This study provides a basis for further investigating the effects of microplastics on mammalian health,especially human health.Methods:Healthy 25-30 g Kunming mice were acclimated for a week.Each male mouse was randomly caged with 2 female mice overnight.The mice with vaginal plug formation on following morning were identified as conception.During pregnancy and lactation,the dams in the three study groups drank water containing 0.1mg/L(low dose),1 mg/L(medium dose)and 10 mg/L(high dose)PS-NPs(100 nm),respectively.The control group only drank the deionized water.On postnatal day(PND)21 and 56,the liver,testis,kidney,small intestine and serum were collected from the male pups.The histopathological changes of liver,testis,kidney and small intestine were observed by HE staining.The activities of aspartate aminotransferase(AST)and alanine aminotransferase(ALT)in serum were detected by microplate method.The content of Malonaldehyde(MDA)and activities of catalase(CAT)and superoxide dismutase(SOD)in the liver and testis were determined by spectrophotometry.The expression of interleukin-6(IL-6),tumor necrosis factor-α(TNF-α)and interleukin-1β(IL-1β)in liver were detected by real-time fluorescence quantitative PCR.The energy metabolites in liver tissue were detected by targeted metabolomics.Furthermore,the epididymides were collected and sperm count was performed on PND 56.Results:(1)Maternal PS-NPs exposure during pregnancy and lactation led to growth retardation in offspring mice.Compared with the control group,the birth weight and body weight on PND 56 in medium-dose and high-dose PS-NPs exposure groups obviously decreased(P < 0.05).Meanwhile,the body weight in all the three PS-NPs exposure groups significantly decreased on PND 21(P < 0.05).In addition,the percent of offspring mice opening eyes in high-dose PS-NPs exposure group was significantly lower than that in the control group(P < 0.05).(2)Maternal PS-NPs exposure during pregnancy and lactation altered liver histology in male offspring mice.Compared with the control group,the liver volume and weight of male progeny mice in medium-and high-dose PS-NPs exposure groups significantly decreased on PND21(P < 0.05).Furthermore,more yellowish-white punctate lesions were found on the surface of liver in the high-dose PS-NPs exposed group.Histological examination showed hepatic architecture distortion and massive inflammatory cell infiltration in high-dose PS-NPs exposure group.However,on PND 56,the relative liver weight of male progeny mice in the medium-and high-dose PS-NPs exposure group was higher than that in the control group(P < 0.05).No punctate lesions and inflammatory cell infiltration were observed in the liver tissue.(3)Maternal PS-NPs exposure during pregnancy and lactation induced oxidative stress in the liver tissue of male offspring mice.On PND 21,compared with the control group,high-dose PS-NPs exposure significantly increased the generation of MDA and reduced the activities of CAT and SOD in the liver of offspring mice(P< 0.05).On PND 56,MDA content and CAT and SOD activities in the liver of male offspring in high-dose PS-NPs group was higher than that in the control group(P <0.05).(4)Maternal PS-NPs exposure during pregnancy and lactation up-regulated the expression of proinflammatory factors in the liver of male offspring mice.On PND21,the expression of IL-6,TNF-α and IL-1β was significantly up-regulated in the high-dose PS-NPs exposure group(P < 0.05).However,On PND 56,all doses of PS-NPs had no significant effects on the expression of IL-6,TNF-α and IL-1β genes in the liver of male offspring(P > 0.05).(5)Maternal PS-NPs exposure during pregnancy and lactation caused the disorder of energy metabolism in the liver of male offspring mice.Compared with the control group,high-dose PS-NPs exposure significantly decreased the levels of dihydroxyacetone phosphate,β-D-fructose 6-phosphate,adenosine monophosphate,D-glucose 6-phosphate and thiamine pyrophosphate in the liver of offspring mice(P< 0.05).(6)Maternal PS-NPs exposure during pregnancy and lactation altered the histology of testis in offspring mice.On PND 21,the testicular weight and the relative testicular weight in the high-dose PS-NPs exposure group significantly decreased when compared to the control group(P < 0.05).On PND 56,the testicular weight in medium-dose and high-dose PS-NPs exposed group decreased compared with the control group(P < 0.05),while the relative testicular weight had no significant change(P > 0.05).Histological examination showed loose testicular interstitium,decreased seminiferous epithelium layers,detachment of spermatogenic cells,and reduced sperm number in the lumen in medium-and high-dose PS-NPs exposure groups.On PND 56,the sperm count in epididymis in the medium-and high-dose PS-NPs exposure groups was significantly lower than that in the control group(P <0.05).(7)Maternal PS-NPs exposure during pregnancy and lactation induced oxidative stress in testis of offspring mice.On PND21,the content of MDA in the testis of progeny mice increased and the activity of SOD decreased in high-dose PS-NPs exposure group,compared with the control group(P < 0.05).The testicular activity of CAT in medium-and high-dose PS-NPs exposure group were significantly lower than that in the control group(P < 0.05).On PND 56,high-dose PS-NPs exposure enhanced MDA production.At the same time,the testicular activity of CAT and SOD increased in medium-and high-dose PS-NPs exposure groups(P < 0.05).Conclusion:(1)PS-NPs has developmental toxicity,and maternal PS-NPs exposure during pregnancy and lactation can lead to growth retardation in offspring mice.(2)Maternal PS-NPs exposure can induce oxidative stress,inflammatory response and glycometabolism disorders,leading to hepatotoxic damage in male offspring mice.(3)Testis is one of the targets of PS-NPs toxicity.Maternal PS-NPs exposure can induce oxidative stress in the testis of offspring mice,resulting in testicular toxic damage and spermatogenesis disorder in offspring mice. |
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