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Polystyrene microplastic-induced endoplasmic reticulum stress contributes to growth plate endochondral ossification
Qingqing Zhang1, Yuanyuan Lang2, Xiaomin Tang1
1Department of Pediatrics, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, People's Republic of China.
Background:
Previous studies on the effects of microplastics (MPs) on bone in early development are limited. This study aimed to investigate the adverse effects of MPs on bone in young rats and the potential mechanism.
Methods:
Three-week-old female rats were orally administered MPs for 28 days, and endoplasmic reticulum (ER) stress inhibitor salubrinal (SAL) and ER stress agonist tunicamycin (TM) were added to evaluate the effect of ER stress on toxicity of MPs. The indicators of growth and plasma markers of bone turnover were evaluated. Tibias were analyzed using micro-computed tomography (micro-CT). Histomorphological staining of growth plates was performed, and related gene expression of growth plate chondrocytes was tested.
Results:
After exposure of MPs, the rats had decreased growth, shortened tibial length, and altered blood calcium and phosphorus metabolism. Trabecular bone was sparse according to micro-CT inspection. In the growth plate, the thickness of proliferative zone substantial reduced while the thickness of hypertrophic zone increased significantly, and the chondrocytes were scarce and irregularly arranged according to tibial histological staining. The transcription of the ER stress-related genes BIP, PERK, ATF4, and CHOP dramatically increased, and the transcription factors involved in chondrocyte proliferation, differentiation, apoptosis, and matrix secretion were aberrant according to RT-qPCR and western blotting. Moreover, the addition of TM showed higher percentage of chondrocyte death. Administration of SAL alleviated all of the MPs-induced symptoms.
Conclusion:
These results indicated that MPs could induce growth retardation and longitudinal bone damage in early development. The toxicity of MPs may attribute to induced ER stress and impaired essential processes of the endochondral ossification after MPs exposure.
Insights
Microplastics (MPs) exposure in young rats caused growth retardation and bone damage by inducing endoplasmic reticulum (ER) stress. Salubrinal (SAL) treatment alleviated these adverse effects, suggesting ER stress is a key mechanism.
Area of Science:
- Environmental Toxicology
- Developmental Biology
- Bone Biology
Background:
- Limited research exists on microplastic (MP) effects on bone during early development.
- This study investigates the impact of MPs on bone health in young rats and elucidates the underlying mechanisms.
Purpose of the Study:
- To assess the adverse effects of microplastic exposure on bone development in young rats.
- To explore the role of endoplasmic reticulum (ER) stress in mediating microplastic toxicity on bone.
Main Methods:
- Young female rats were exposed to MPs orally for 28 days.
- Endoplasmic reticulum (ER) stress modulators (salubrinal and tunicamycin) were used to evaluate ER stress involvement.
- Bone growth, turnover markers, micro-computed tomography (micro-CT), histomorphology, and gene expression analysis were performed.
Main Results:
- MP exposure led to decreased growth, shortened tibias, and altered calcium/phosphorus metabolism.
- Micro-CT revealed sparse trabecular bone, while histology showed growth plate abnormalities and chondrocyte disorganization.
- Increased ER stress gene expression (BIP, PERK, ATF4, CHOP) and aberrant chondrocyte-related transcription factors were observed.
- Tunicamycin exacerbated chondrocyte death, while salubrinal treatment ameliorated MP-induced symptoms.
Conclusions:
- Microplastics induce growth retardation and longitudinal bone damage in early development.
- Microplastic toxicity is linked to induced endoplasmic reticulum (ER) stress, impairing endochondral ossification.
- Targeting ER stress pathways may offer a therapeutic strategy against microplastic-induced bone damage.
