
Health Rounds: Widely used pain drug can be made from plastic waste
Common bacteria can turn plastic waste into the over-the-counter painkiller acetaminophen, researchers have discovered.
Acetaminophen, the main ingredient in Tylenol and also known as paracetamol in some countries, is usually made from fossil fuels.
The new method, developed with support from AstraZeneca (AZN.L), opens new tab, transforms a molecule from a widely used plastic known as polyethylene terephthalate (PET) into Tylenol's active ingredient, leaving virtually no carbon emissions, according to a report in Nature Chemistry, opens new tab.
The plastic is converted to the drug at room temperature in less than 24 hours, using a fermentation process similar to what is used in brewing beer, the researchers said.
PET, a strong, lightweight plastic used for water bottles and food packaging, accounts for more than 350 million tons of waste annually.
'This work demonstrates that PET plastic isn't just waste or a material destined to become more plastic. It can be transformed by microorganisms into valuable new products, including those with potential for treating disease,' study leader Stephen Wallace of the University of Edinburgh said in a statement.
More work is needed before PET can be used to produce acetaminophen at commercial levels, the researchers said.
The majority of men and women have microplastics in their reproductive fluids, according to the results of a small study, opens new tab reported at the European Society of Human Reproduction and Embryology, opens new tab meeting in Paris.
The presence of the microplastics raises important questions about their potential risks to fertility and reproductive health, researchers said.
The tiny contaminants – plastic particles under 5 millimeters in size – were present in the follicular fluid that encases developing eggs in the ovaries in 20 of 29 women, or 69%. Microplastics were found in seminal fluid in 12 of 22 men, or 55%.
Both types of fluid play critical roles in natural conception and assisted reproduction, the researchers said.
In both groups, the microplastic polymers included polytetrafluoroethylene (Teflon), polystyrene, polyethylene terephthalate, polyamide, polypropylene and polyurethane.
In animals, microplastics can induce inflammation, damage to tissues and to DNA, and hormonal disruptions, study leader Emilio Gomez-Sanchez of Next Fertility Murcia in Spain said in a statement.
In a separate presentation, opens new tab at the meeting, Manel Boussabeh of Fattouma Bourguiba Hospital in Monastir, Tunisia, and colleagues reported that sperm exposed to microplastics in test tubes had impaired motility and damage to DNA.
Other researchers have previously found, opens new tab significant amounts of microplastics in the testicles of dogs and humans, and the canine data suggested the particles may contribute to impaired fertility.
Researchers can turn off chronic inflammation while leaving intact the ability of cells to respond to short-term injuries and illnesses by targeting a newly identified protein, according to a report in Nature, opens new tab.
Chronic inflammation occurs when the immune system is stuck in overdrive, as with persistent conditions such as arthritis, inflammatory bowel disease or obesity. Acute inflammation – with pain, fever, swelling, and redness, for example – resolves relatively quickly.
Researchers found that a protein responsible for controlling inflammatory genes becomes degraded and is lost from cells during chronic inflammation.
In test tube experiments, restoring the protein called WSTF blocked chronic inflammation in human cells without interfering with acute inflammation, allowing appropriate immune responses to short-term threats.
The researchers then designed a medicine that protects WSTF from degradation and suppresses chronic inflammation by blocking the WSTF interaction with another protein in the cell nucleus.
The researchers have successfully tested the drug to treat mice with fatty liver disease or arthritis and to reduce inflammation in chronically inflamed knee cells obtained from patients undergoing joint replacement surgery.
Studying human tissue samples, the researchers found that WSTF is lost in the livers of patients with fatty liver disease but not in the livers of healthy people.
'Chronic inflammatory diseases cause a great deal of suffering and death, but we still have much to learn about what drives chronic inflammation and how to treat it,' study leader Zhixun Dou of Massachusetts General Hospital said in a statement.
'Our findings help us separate chronic and acute inflammation, as well as identify a new target for stopping chronic inflammation that results from aging and disease.'
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Focusing on cancer drugs letrozole and irinotecanFor this study, researchers began by using past studies to assess how Alzheimer's disease changed gene expression in brain cells, mainly neurons and glia. 'Glia cells are non-neuronal cells that provide support and protection to neurons in the nervous system,' Sirota explained. 'By targeting both neuronal cells and non-neuronal cells (glia) we hope to be able to more comprehensively target disease pathophysiology.' From there, scientists then took the gene expression signatures they found and used a database called the ConnectivityMap, allowing them to examine thousands of drugs to find ones that reversed the Alzheimer's disease gene expression signature.'We started with a set of 1,300 drugs and narrowed it down to the combination of letrozole and irinotecan through data driven analysis using both molecular and clinical data,' Sirota said.'We first identified compounds that reversed the cell type specific disease signatures back to normal based on the gene expression profiles. We then further filtered the list to the candidates that affect several cell types,' she explained.'Then we wanted to see whether patients who are on those drugs already have a lower risk of Alzheimer's disease by querying electronic medical records across the UC system,' she continued. 'This has allowed us to narrow our list down to a handful of drugs and focus on this combination.' 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'This tells us that multiple levels of evidence — molecular data, clinical information and mouse model experiments are all aligning to tell us that these compounds might be helpful for Alzheimer's disease patients,' Sirota further noted that:'While we don't know the exact mechanism of how these drugs work to treat Alzheimer's disease, we know that irinotecan is a chemotherapy drug that works by inhibiting the enzyme DNA topoisomerase I, specifically targeting the S and G2 phases of the cell cycle. Letrozole's mechanism of action involves inhibiting the enzyme aromatase, which is crucial in the biosynthesis of estrogen.''However, we don't know whether it is the main aforementioned mechanisms or off-target effects of these drugs which might help Alzheimer's disease patients,' Sirota cautioned. 'Additional experiments need to be carried out to better understand how these two drugs might work together to combat Alzheimer's disease in patients.'Using 'big data' and inventive approaches to find potential Alzheimer's drug targetsMNT had the opportunity to speak with John Dickson, MD, PhD, a neurologist at Massachusetts General Hospital, about this research. 'This is an interesting and innovative paper that uses 'big data' to aid in identifying potential drug targets to treat Alzheimer's disease and then tests candidates in a preclinical model of Alzheimer's disease,' Dickson, who was not involved in this research, said.'Combining the use of transcriptomic data from brain tissue from Alzheimer's disease patients, drug perturbation studies in cell lines, and patient data from electronic medical records was an inventive approach to identifying and narrowing down potential drug targets,' he Dickson's view, 'the decision to use a dual-therapy approach and plan to target multiple cell types with this strategy was also innovative.''The combination of drugs showed beneficial effects on the memory testing and neuropathological findings in a mouse model of Alzheimer's disease. In addition to identifying two potential candidate therapies for Alzheimer's disease, this paper also provides an experimental paradigm for identifying new drugs to treat a variety of conditions,' he look at repurposing existing drugs for Alzheimer's treatment? MNT also talked to Clifford Segil, DO, a neurologist at Providence Saint John's Health Center in Santa Monica, CA, about this study, who said it is refreshing to see data that supports improving memory loss through a novel mechanism that is not related to current therapies that work on brain acetylcholine, N-methyl-D-aspartate (NMDA), or amyloid.'This study's design is smart and the data is captivating,' Segil, who likewise was not involved in the research, added. 'Repurposing medications already being used has been extremely rewarding in neurologists and I truly hope something grows out of this research.' And Peter Gliebus, MD, neurologist and director of cognitive and behavioral neurology at Marcus Neuroscience Institute, part of Baptist Health South Florida, also not involved in the research, commented to MNT that this was a promising and exciting study, and said that repurposing existing drugs offers several advantages. 'Faster development since these drugs already have established safety profiles, which reduces the time and cost required for clinical trials,' Gliebus noted.'Cost-effectiveness [is achieved] by avoiding the high expenses associated with developing new drugs from scratch. And [this approach has] a broader impact, as many existing drugs may have unexplored mechanisms that could address complex Alzheimer's disease pathologies, such as neuroinflammation, synaptic dysfunction, and metabolic deficits.''Given the high failure rate of Alzheimer's drug trials, repurposing provides a practical and efficient pathway to identify effective treatments,' the neurologist concluded.