Qingfeng Zhai
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Qingfeng Zhai has a total of 66 co-authors. Here are the top co-authors by number of shared publications:
Ruoyu Zhang
School of Public Health Hebei Medical University Shijiazhuang China
4 shared publicationsFeiyan Tao
School of Public Health, Weifang Medical University, Weifang 261053, China
3 shared publicationsRuolan You
School of Public Health, Shandong Second Medical University, Weifang, 261053, China
3 shared publicationsXianzhi He
School of Public Health, Changsha Medical University, Changsha 410219, China
3 shared publicationsYuxin Li
School of Public Health, Weifang Medical University, Weifang 261053, China
3 shared publicationsJiaqi Zhou
School of Public Health, Shandong Second Medical University, Weifang, 261053, China
2 shared publications
Latest Publications
- 2 January 2026
- Published by Elsevier in Environmental Pollution
- Vol. 392, 127631
Differential organ-specific toxicity profiling of BDE-209 and its derivative DBDPE in zebrafish
- 2 January 2026
- Published by Elsevier in Environmental Pollution
- Vol. 392, 127631
Differential organ-specific toxicity profiling of BDE-209 and its derivative DBDPE in zebrafish
- 25 December 2025
- Published by Elsevier in Reproductive Toxicology
- Vol. 140, 109152
Childhood susceptibility to PFAS-associated endocrine disruption: NHANES age-stratified analysis and PFOS mouse model validation
- 25 December 2025
- Published by Elsevier in Reproductive Toxicology
- Vol. 140, 109152
Childhood susceptibility to PFAS-associated endocrine disruption: NHANES age-stratified analysis and PFOS mouse model validation
- Open Access
- 10 September 2025
- Published by Elsevier in Ecotoxicology and Environmental Safety
- Vol. 303, 119021
Micro- and nano-plastic contamination in foods and potential risk to human health
- 10 September 2025
- Published by Elsevier in Ecotoxicology and Environmental Safety
- Vol. 303, 119021
Open AccessMicro- and nano-plastic contamination in foods and potential risk to human health
- Open Access
- 23 April 2025
- Published by Frontiers Media SA in Frontiers in Neuroscience
- Vol. 19, 1576773
Role and mechanism of molecular hydrogen in the treatment of Parkinson’s diseases
Parkinson’s disease (PD) is a complex neurodegenerative disorder characterized by a pathology that includes the aggregation of alpha-synuclein (α-syn), oxidative stress, and neuroinflammation. While existing treatments can alleviate motor symptoms, they have limited efficacy in slowing disease progression and improving non-motor symptoms. In recent years, molecular hydrogen has been recognized for its potential neuroprotective effects, attributed to its selective antioxidant and anti-inflammatory properties. While preclinical studies demonstrate promising results, clinical trials conducted thus far have yielded mixed outcomes, with some trials reporting limited or no therapeutic benefit. This review systematically analyzes the mechanisms of action of molecular hydrogen in PD and related neurodegenerative disorders, emphasizing its antioxidant, anti-inflammatory, and anti-apoptotic properties. By evaluating evidence from both preclinical and clinical studies, this paper explores the potential of molecular hydrogen to attenuate oxidative stress, modulate inflammatory responses, and inhibit apoptosis in neuronal cells, while also identifying key gaps in current research. As a novel neuroprotective agent, molecular hydrogen holds potential in PD and other neurodegenerative diseases, but further well-designed clinical trials are needed to validate its efficacy. Future studies should focus on elucidating the mechanisms through which hydrogen exerts its neuroprotective effects, particularly concerning α-syn aggregation and its clearance pathways, as well as Nrf2-mediated immunomodulation. Furthermore, large-scale, multicenter clinical trials are necessary to establish efficacy benchmarks and personalized delivery protocols.
- 23 April 2025
- Published by Frontiers Media SA in Frontiers in Neuroscience
- Vol. 19, 1576773
Open AccessRole and mechanism of molecular hydrogen in the treatment of Parkinson’s diseases
Parkinson’s disease (PD) is a complex neurodegenerative disorder characterized by a pathology that includes the aggregation of alpha-synuclein (α-syn), oxidative stress, and neuroinflammation. While existing treatments can alleviate motor symptoms, they have limited efficacy in slowing disease progression and improving non-motor symptoms. In recent years, molecular hydrogen has been recognized for its potential neuroprotective effects, attributed to its selective antioxidant and anti-inflammatory properties. While preclinical studies demonstrate promising results, clinical trials conducted thus far have yielded mixed outcomes, with some trials reporting limited or no therapeutic benefit. This review systematically analyzes the mechanisms of action of molecular hydrogen in PD and related neurodegenerative disorders, emphasizing its antioxidant, anti-inflammatory, and anti-apoptotic properties. By evaluating evidence from both preclinical and clinical studies, this paper explores the potential of molecular hydrogen to attenuate oxidative stress, modulate inflammatory responses, and inhibit apoptosis in neuronal cells, while also identifying key gaps in current research. As a novel neuroprotective agent, molecular hydrogen holds potential in PD and other neurodegenerative diseases, but further well-designed clinical trials are needed to validate its efficacy. Future studies should focus on elucidating the mechanisms through which hydrogen exerts its neuroprotective effects, particularly concerning α-syn aggregation and its clearance pathways, as well as Nrf2-mediated immunomodulation. Furthermore, large-scale, multicenter clinical trials are necessary to establish efficacy benchmarks and personalized delivery protocols.
- 18 March 2025
- Published by Elsevier in Journal of Hazardous Materials
- Vol. 491, 137989
An occupational health assessment of dinotefuran exposure in greenhouse vegetable workers: Metabolomic profiling and toxicokinetic analysis
- 18 March 2025
- Published by Elsevier in Journal of Hazardous Materials
- Vol. 491, 137989
An occupational health assessment of dinotefuran exposure in greenhouse vegetable workers: Metabolomic profiling and toxicokinetic analysis
- Open Access
- 21 October 2024
- Published by Wiley in The Clinical Respiratory Journal
- Vol. 18 (10) , e70030
The Relationship of Vitamin A and Neonatal Respiratory Diseases: A Meta‐Analysis
This study systematically analyzes the relationship of vitamin A on the neonatal respiratory diseases. An extensive literature search for relevant studies was conducted on PubMed, Web of Science, and so on. After screening in strict accordance with the inclusion and exclusion criteria, 12 articles on vitamin A deficiency and 12 articles on vitamin A supplementation were included. Stata 17.0 software was used to perform meta‐analysis, heterogeneity test, and sensitivity analysis, and the corresponding mathematical model was used to merge the data. The meta‐analysis results of the relationship between vitamin A deficiency and neonatal respiratory diseases indicated that compared with the neonates with normal vitamin A, the neonates with vitamin A deficiency had adverse health outcomes of neonatal respiratory diseases (OR = 4.86, 95% CI: 2.68–8.84), of which neonatal respiratory distress syndrome (NRDS) (OR = 4.10, 95% CI: 2.32–7.23) and neonatal pneumonia (OR = 3.22, 95% CI: 2.18–4.77) were analyzed by subgroup analysis. The meta‐analysis of the relationship between vitamin A supplementation therapy and neonatal respiratory diseases showed that vitamin A supplementation was an effective therapeutic measure for neonatal respiratory diseases (RR = 1.06, 95% CI: 1.04–1.07): NRDS (RR = 1.03, 95% CI: 1.02–1.05) and NBPD (RR = 1.08, 95% CI: 1.01–1.15). The funnel chart method results show that there was publication bias in studies on vitamin A deficiency induced to and vitamin A supplementation therapy for neonatal respiratory diseases. The sensitivity analysis results showed that excluding some special article had some effect on the final pooled effect. But generally speaking, the result of meta‐analysis was stable. There is a statistical correlation of vitamin A on the neonatal respiratory diseases from two aspects of etiological exploration and effect evaluation of treatment.
- 21 October 2024
- Published by Wiley in The Clinical Respiratory Journal
- Vol. 18 (10) , e70030
Open AccessThe Relationship of Vitamin A and Neonatal Respiratory Diseases: A Meta‐Analysis
This study systematically analyzes the relationship of vitamin A on the neonatal respiratory diseases. An extensive literature search for relevant studies was conducted on PubMed, Web of Science, and so on. After screening in strict accordance with the inclusion and exclusion criteria, 12 articles on vitamin A deficiency and 12 articles on vitamin A supplementation were included. Stata 17.0 software was used to perform meta‐analysis, heterogeneity test, and sensitivity analysis, and the corresponding mathematical model was used to merge the data. The meta‐analysis results of the relationship between vitamin A deficiency and neonatal respiratory diseases indicated that compared with the neonates with normal vitamin A, the neonates with vitamin A deficiency had adverse health outcomes of neonatal respiratory diseases (OR = 4.86, 95% CI: 2.68–8.84), of which neonatal respiratory distress syndrome (NRDS) (OR = 4.10, 95% CI: 2.32–7.23) and neonatal pneumonia (OR = 3.22, 95% CI: 2.18–4.77) were analyzed by subgroup analysis. The meta‐analysis of the relationship between vitamin A supplementation therapy and neonatal respiratory diseases showed that vitamin A supplementation was an effective therapeutic measure for neonatal respiratory diseases (RR = 1.06, 95% CI: 1.04–1.07): NRDS (RR = 1.03, 95% CI: 1.02–1.05) and NBPD (RR = 1.08, 95% CI: 1.01–1.15). The funnel chart method results show that there was publication bias in studies on vitamin A deficiency induced to and vitamin A supplementation therapy for neonatal respiratory diseases. The sensitivity analysis results showed that excluding some special article had some effect on the final pooled effect. But generally speaking, the result of meta‐analysis was stable. There is a statistical correlation of vitamin A on the neonatal respiratory diseases from two aspects of etiological exploration and effect evaluation of treatment.
- 21 April 2024
- Published by Elsevier in Toxicology
- Vol. 505, 153810
Ferroptosis is involved in trophoblast cells cytotoxicity induced by black phosphorus nanoparticles
- 21 April 2024
- Published by Elsevier in Toxicology
- Vol. 505, 153810
Ferroptosis is involved in trophoblast cells cytotoxicity induced by black phosphorus nanoparticles
- Open Access
- 5 September 2023
- Published by Elsevier in Ecotoxicology and Environmental Safety
- Vol. 264, 115429
Safety evaluation of rare ginsenosides of stems and leaves from American ginseng: 90-day exposure toxicity study combined with intestinal flora analysis and metabonomics in rats
- 5 September 2023
- Published by Elsevier in Ecotoxicology and Environmental Safety
- Vol. 264, 115429
Open AccessSafety evaluation of rare ginsenosides of stems and leaves from American ginseng: 90-day exposure toxicity study combined with intestinal flora analysis and metabonomics in rats
- Open Access
- 1 July 2023
- Published by Springer Nature in Environmental Science and Pollution Research
- Vol. 30 (37) , 88238
Correction to: Answer to “Comments” on “The combined effect of titanium dioxide nanoparticles and cypermethrin on male reproductive toxicity in rats” by Armen Nersesyan et al., https://doi.org/10.1007/s11356-022-23796-x
- 1 July 2023
- Published by Springer Nature in Environmental Science and Pollution Research
- Vol. 30 (37) , 88238
Open AccessCorrection to: Answer to “Comments” on “The combined effect of titanium dioxide nanoparticles and cypermethrin on male reproductive toxicity in rats” by Armen Nersesyan et al., https://doi.org/10.1007/s11356-022-23796-x