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<p>Medicines, food packaging, personal care products, and cosmetics extensively use polyethylene terephthalate nanoplastics (PET-NaPs). However, they also have harmful impacts on several organs. Betaine demonstrates potent antioxidant and anti-inflammatory characteristics. Our goal was to investigate the detrimental impact of PET-NaPs on the mouse brain and evaluate the neuroprotective properties of betaine. We allocated 40 completely mature male Swiss albino mice into four distinct groups: control group, betaine group, PET-NaPs group, and betaine-co-treated group. Following a 30-day duration, euthanasia was performed on the mice, and analyzed tissue samples were obtained from the cerebrum, cerebellum, and hippocampus. PET-NaPs resulted in an elevated level of malondialdehyde and upregulated cyclooxygenase-2 and interleukin-1 beta (IL-1β) expression while significantly reducing the levels of glutathione and downregulating acetylcholinesterase. The PET-NPs also caused significant changes in the histopathology of the brain tissue, and there was a demonstrable rise in the immunostaining of IL-1β and glial fibrillary acidic proteins. Consequently, betaine effectively alleviated the negative consequences of PET-NaPs. Therefore, betaine possesses the capacity to mitigate the neurotoxic consequences induced by PET-NaPs.</p>

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Polyethylene terephthalate nanoplastics-induced neurotoxicity in adult male Swiss albino mice with amelioration of betaine: a histopathological, neurochemical, and molecular investigation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月12日

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  • Nehal A. Kamel,
  • Dina W. Bashir,
  • Ebtihal M. M. El-Leithy,
  • Adel F. Tohamy,
  • Maha M. Rashad,
  • Ghada E. Ali,
  • Abdel Aleem A. El-Saba

摘要

Medicines, food packaging, personal care products, and cosmetics extensively use polyethylene terephthalate nanoplastics (PET-NaPs). However, they also have harmful impacts on several organs. Betaine demonstrates potent antioxidant and anti-inflammatory characteristics. Our goal was to investigate the detrimental impact of PET-NaPs on the mouse brain and evaluate the neuroprotective properties of betaine. We allocated 40 completely mature male Swiss albino mice into four distinct groups: control group, betaine group, PET-NaPs group, and betaine-co-treated group. Following a 30-day duration, euthanasia was performed on the mice, and analyzed tissue samples were obtained from the cerebrum, cerebellum, and hippocampus. PET-NaPs resulted in an elevated level of malondialdehyde and upregulated cyclooxygenase-2 and interleukin-1 beta (IL-1β) expression while significantly reducing the levels of glutathione and downregulating acetylcholinesterase. The PET-NPs also caused significant changes in the histopathology of the brain tissue, and there was a demonstrable rise in the immunostaining of IL-1β and glial fibrillary acidic proteins. Consequently, betaine effectively alleviated the negative consequences of PET-NaPs. Therefore, betaine possesses the capacity to mitigate the neurotoxic consequences induced by PET-NaPs.