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Innovation: Benzophenones compounds are widely added to sunscreen and other skin care products because of their good UV absorption properties, and they have been widely detected in human tissues including the placenta
.
The early birth cohort study of Professor Xu Shunqing’s team found that one of the main metabolites of benzophenone, tetrahydroxybenzophenone (4HBP), had the same level of exposure during the mother’s pregnancy as the child’s mental development at 2 years old.
Significant negative correlation suggests that early exposure to benzophenone may have neurodevelopmental toxicity
.
This study reveals the mechanism by which 4HBP induces developmental defects in the hippocampus and impaired cognitive function by inducing the imbalance of endoplasmic reticulum protein homeostasis and inflammation, suggesting that the use of nursing products containing benzophenones during pregnancy may affect offspring Neurodevelopment provides a theoretical basis at the molecular level for preventing the neurodevelopmental toxicity of benzophenone
.
Keywords: tetrahydroxybenzophenone, early life exposure, neurodevelopmental toxicity, endoplasmic reticulum protein homeostasis
.
The impact of exposure to environmental pollutants in early life on children’s neurodevelopment has received increasing attention in recent years
.
Benzophenone has good UV absorption properties and is widely used in sunscreen skin care products, food packaging coatings and inks, etc.
However, little is known about its neurotoxicity
.
The team of Professor Xu Shunqing of Huazhong University of Science and Technology built a large mother-infant cohort in the early stage and found that the exposure level of 4HBP, the main metabolite of benzophenone, in pregnant mothers was significantly negatively correlated with the offspring’s intellectual development at the age of 2 years, suggesting benzophenones The compound may have neurodevelopmental toxicity
.
In order to confirm the toxic effect and explore its molecular mechanism, the research team first treated pregnant mice with 4HBP throughout the pregnancy to simulate human exposure during pregnancy
.
After testing, the internal exposure level of the mice after 1 mg/kg/day treatment was close to that of the population
.
The offspring mice were bred under normal conditions to 56 days of age after birth
.
Obvious memory and learning disabilities can be observed in behavioral experiments .
Immunofluorescence staining verified the changes in hippocampus development and the effects on neural stem cell function after exposure
.
Interestingly, no obvious abnormalities were observed when the adult mice were exposed to the same dose and time, suggesting that the early stage of neurodevelopment may be the window period for the toxic effects of 4HBP
.
Transcriptome sequencing of infected neural stem cells found that 4HBP mainly affects the proliferation of neural stem cells rather than differentiation.
Among them, the endoplasmic reticulum stress-induced apoptosis signals and inflammatory response-related pathways are significantly enriched
.
Scanning electron microscopy observed abnormal endoplasmic reticulum morphology in neural stem cells after exposure, indicating that they were in a state of stress
.
Detection of gene and protein levels revealed that PERK signal, one of the main pathways to maintain the homeostasis of endoplasmic reticulum proteins, and NFκB signal, a key pathway that regulates inflammatory response, were significantly activated
.
A series of subsequent molecular biology experiments revealed that the transcription factor ATF4 downstream of the PERK signal can activate the expression of p65 in the NFκB complex at the transcriptional level, promote inflammation and cell apoptosis, and thereby mediate the toxic effects of 4HBP
.
Next, the researchers further verified whether inhibition of the PERK pathway can improve hippocampal developmental defects caused by 4HBP
.
Based on this hypothesis, the research team used neural stem cells, mice, and human brain-like organs to specifically inhibit the activation of the PERK pathway through RNA interference and small molecule inhibitors
.
The results showed that the cytotoxic effect, the cognitive ability of offspring mice and the development of human brain-like organs were all significantly improved
.
These results indicate that benzophenone exposure during pregnancy can induce apoptosis of neural stem cells by disturbing the homeostasis of endoplasmic reticulum proteins, leading to developmental defects in the hippocampus of offspring and impaired cognitive function
.
The study suggests that the use of nursing products containing benzophenones during pregnancy may affect the neurodevelopment of offspring, providing a molecular level scientific basis for the neurodevelopmental toxicity induced by benzophenone
.
Related work was published in Advanced Science (DOI: 10.
1002/advs.
202102686) under the title "Maternal benzophenone exposure impairs hippocampus development and cognitive function in mouse offspring"
.
Associate Professor Sheng Xia and Professor Xu Shunqing, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, and Assistant Professor Tang Yaohui, School of Biomedical Engineering, Shanghai Jiaotong University, are the co-corresponding authors of this article
.
Cui Fengzhen, a doctoral student in the Shengxia research group, and Dr.
Qingfei Pan from the St.
Jude Children’s Research Hospital in the United States are the co-first authors
.
WILEY paper information: Maternal benzophenone exposure impairs hippocampus development and cognitive function in mouse offspringFengzhen Cui#, Qingfei Pan#, Siyi Wang, Faming Zhao, Runxin Wang, Tingting Zhang, Yaying Song, Jun He, Haolin Zhang, Qiang Weng, Yang Jin, Wei Xia, Yuanyuan Li, Guo-Yuan Yang, Winnok De Vos, Jean-Pierre Timmermans, Shunqing Xu*, Yaohui Tang*, Xia Sheng* Advanced Science DOI: 10.
1002/advs.
202102686 Click "Read the original text" in the lower left corner to view the paper Original text
.
Introduction to AdvancedScience Journal "Advanced Science" (Advanced Science) Wiley is a high-quality open source journal founded in 2014.
It publishes innovative achievements and cutting-edge progress in various fields such as materials science, physical chemistry, biomedicine, and engineering
.
The journal is dedicated to disseminating scientific research results to the public to the greatest extent, and all articles are freely available
.
The latest impact factor is 16.
806, and the 2020 SCI journals of the Chinese Academy of Sciences will be divided into the Q1 area of the material science category and the Q1 area of the engineering technology category
.
Press and hold the QR code on the official WeChat platform of AdvancedScienceNewsWiley's scientific research information.
Follow us to share cutting-edge information｜Focus on scientific research trends to publish scientific research news or apply for information sharing, please contact: ASNChina@Wiley.
com
.
The early birth cohort study of Professor Xu Shunqing’s team found that one of the main metabolites of benzophenone, tetrahydroxybenzophenone (4HBP), had the same level of exposure during the mother’s pregnancy as the child’s mental development at 2 years old.
Significant negative correlation suggests that early exposure to benzophenone may have neurodevelopmental toxicity
.
This study reveals the mechanism by which 4HBP induces developmental defects in the hippocampus and impaired cognitive function by inducing the imbalance of endoplasmic reticulum protein homeostasis and inflammation, suggesting that the use of nursing products containing benzophenones during pregnancy may affect offspring Neurodevelopment provides a theoretical basis at the molecular level for preventing the neurodevelopmental toxicity of benzophenone
.
Keywords: tetrahydroxybenzophenone, early life exposure, neurodevelopmental toxicity, endoplasmic reticulum protein homeostasis
.
The impact of exposure to environmental pollutants in early life on children’s neurodevelopment has received increasing attention in recent years
.
Benzophenone has good UV absorption properties and is widely used in sunscreen skin care products, food packaging coatings and inks, etc.
However, little is known about its neurotoxicity
.
The team of Professor Xu Shunqing of Huazhong University of Science and Technology built a large mother-infant cohort in the early stage and found that the exposure level of 4HBP, the main metabolite of benzophenone, in pregnant mothers was significantly negatively correlated with the offspring’s intellectual development at the age of 2 years, suggesting benzophenones The compound may have neurodevelopmental toxicity
.
In order to confirm the toxic effect and explore its molecular mechanism, the research team first treated pregnant mice with 4HBP throughout the pregnancy to simulate human exposure during pregnancy
.
After testing, the internal exposure level of the mice after 1 mg/kg/day treatment was close to that of the population
.
The offspring mice were bred under normal conditions to 56 days of age after birth
.
Obvious memory and learning disabilities can be observed in behavioral experiments .
Immunofluorescence staining verified the changes in hippocampus development and the effects on neural stem cell function after exposure
.
Interestingly, no obvious abnormalities were observed when the adult mice were exposed to the same dose and time, suggesting that the early stage of neurodevelopment may be the window period for the toxic effects of 4HBP
.
Transcriptome sequencing of infected neural stem cells found that 4HBP mainly affects the proliferation of neural stem cells rather than differentiation.
Among them, the endoplasmic reticulum stress-induced apoptosis signals and inflammatory response-related pathways are significantly enriched
.
Scanning electron microscopy observed abnormal endoplasmic reticulum morphology in neural stem cells after exposure, indicating that they were in a state of stress
.
Detection of gene and protein levels revealed that PERK signal, one of the main pathways to maintain the homeostasis of endoplasmic reticulum proteins, and NFκB signal, a key pathway that regulates inflammatory response, were significantly activated
.
A series of subsequent molecular biology experiments revealed that the transcription factor ATF4 downstream of the PERK signal can activate the expression of p65 in the NFκB complex at the transcriptional level, promote inflammation and cell apoptosis, and thereby mediate the toxic effects of 4HBP
.
Next, the researchers further verified whether inhibition of the PERK pathway can improve hippocampal developmental defects caused by 4HBP
.
Based on this hypothesis, the research team used neural stem cells, mice, and human brain-like organs to specifically inhibit the activation of the PERK pathway through RNA interference and small molecule inhibitors
.
The results showed that the cytotoxic effect, the cognitive ability of offspring mice and the development of human brain-like organs were all significantly improved
.
These results indicate that benzophenone exposure during pregnancy can induce apoptosis of neural stem cells by disturbing the homeostasis of endoplasmic reticulum proteins, leading to developmental defects in the hippocampus of offspring and impaired cognitive function
.
The study suggests that the use of nursing products containing benzophenones during pregnancy may affect the neurodevelopment of offspring, providing a molecular level scientific basis for the neurodevelopmental toxicity induced by benzophenone
.
Related work was published in Advanced Science (DOI: 10.
1002/advs.
202102686) under the title "Maternal benzophenone exposure impairs hippocampus development and cognitive function in mouse offspring"
.
Associate Professor Sheng Xia and Professor Xu Shunqing, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, and Assistant Professor Tang Yaohui, School of Biomedical Engineering, Shanghai Jiaotong University, are the co-corresponding authors of this article
.
Cui Fengzhen, a doctoral student in the Shengxia research group, and Dr.
Qingfei Pan from the St.
Jude Children’s Research Hospital in the United States are the co-first authors
.
WILEY paper information: Maternal benzophenone exposure impairs hippocampus development and cognitive function in mouse offspringFengzhen Cui#, Qingfei Pan#, Siyi Wang, Faming Zhao, Runxin Wang, Tingting Zhang, Yaying Song, Jun He, Haolin Zhang, Qiang Weng, Yang Jin, Wei Xia, Yuanyuan Li, Guo-Yuan Yang, Winnok De Vos, Jean-Pierre Timmermans, Shunqing Xu*, Yaohui Tang*, Xia Sheng* Advanced Science DOI: 10.
1002/advs.
202102686 Click "Read the original text" in the lower left corner to view the paper Original text
.
Introduction to AdvancedScience Journal "Advanced Science" (Advanced Science) Wiley is a high-quality open source journal founded in 2014.
It publishes innovative achievements and cutting-edge progress in various fields such as materials science, physical chemistry, biomedicine, and engineering
.
The journal is dedicated to disseminating scientific research results to the public to the greatest extent, and all articles are freely available
.
The latest impact factor is 16.
806, and the 2020 SCI journals of the Chinese Academy of Sciences will be divided into the Q1 area of the material science category and the Q1 area of the engineering technology category
.
Press and hold the QR code on the official WeChat platform of AdvancedScienceNewsWiley's scientific research information.
Follow us to share cutting-edge information｜Focus on scientific research trends to publish scientific research news or apply for information sharing, please contact: ASNChina@Wiley.
com
