We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Polyethylene terephthalate nanoplastics-induced neurotoxicity in adult male Swiss albino mice with amelioration of betaine: a histopathological, neurochemical, and molecular investigation
Summary
Mice exposed to PET nanoplastics (the type found in food packaging and cosmetics) showed signs of brain damage including increased inflammation, oxidative stress, and reduced levels of a key brain enzyme. The study also found that the supplement betaine significantly protected against this brain damage, suggesting a potential way to counteract nanoplastic-related neurotoxicity.
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.
Sign in to start a discussion.
More Papers Like This
“Polyethylene Terephthalate Nanoplastics Caused Hepatotoxicity in Mice Can be Prevented by Betaine: Molecular and Immunohistochemical Insights”
Researchers found that polyethylene terephthalate nanoplastics caused significant liver damage in mice, including elevated liver enzymes, oxidative stress, and inflammation. When mice were given betaine, a naturally occurring compound, alongside the nanoplastics, the liver damage was substantially reduced. The study suggests that betaine may offer a protective effect against nanoplastic-induced liver toxicity, pointing to potential dietary strategies for mitigating harm from plastic particle exposure.
Screening the Toxic effect of Polyethylene Terephthalate Nanoplastics on Kidney of Adult Male Swiss Albino Mice with Promising Betaine Alleviation
Researchers found that polyethylene terephthalate nanoplastics caused significant kidney damage in mice, including elevated markers of renal stress and structural changes to kidney tissue. The study suggests that pre-treatment with betaine, a naturally occurring compound, may help mitigate some of these harmful effects.
Polyethylene terephthalate (PET) micro- and nanoplastic particles affect the mitochondrial efficiency of human brain vascular pericytes without inducing oxidative stress
Researchers exposed human brain blood vessel cells to PET plastic particles (the same plastic used in water bottles) at micro and nano sizes. After three days, the cells showed reduced energy production in their mitochondria, the powerhouses of the cell, but recovered by six days. While no oxidative stress or cell death was observed, the temporary disruption of brain cell energy production raises questions about what repeated or chronic exposure might do.
Elucidating the Neurotoxicopathological Impact of Micro and Nanoplastics: Mechanistic Insights Into Oxidative Stress-mediated Neurodegeneration and Implications for Public Health in a Plastic Pervasive Era
Researchers reviewed the growing evidence linking micro- and nanoplastic exposure to neurodegenerative diseases, identifying oxidative stress, neuroinflammation, DNA damage, and protein misfolding as key mechanisms of harm to the brain. The review highlights critical knowledge gaps — especially around chronic low-dose exposure — and calls for better detection tools and public health policies to address the emerging neurological threat from plastic pollution.
The plastic brain: neurotoxicity of micro- and nanoplastics
This review examines the emerging evidence that micro- and nanoplastics can reach the brain in both aquatic animals and mammals, potentially causing neurotoxic effects. Researchers found that exposure to these particles induces oxidative stress, inhibits key enzymes involved in nerve signaling, and alters neurotransmitter levels, which may contribute to behavioral changes. The study highlights that systematic research comparing different particle types, sizes, and exposure conditions is urgently needed to understand the neurological risks.