ABSTRACT
Applications for plastic polymers can be found all around the world, often discarded without any prior care, exacerbating the environmental issue. When large waste materials are released into the environment, they undergo physical, biological, and photo-degradation processes that break them down into smaller polymer fragments known as microplastics (MPs). The time it takes for residual plastic to degrade depends on the type of polymer and environmental factors, with some taking as long as 600 years or more. Due to their small size, microplastics can contaminate food and enter the human body through food chains and webs, causing gastrointestinal (GI) tract pain that can range from local to systemic. Microplastics can also acquire hydrophobic organic pollutants and heavy metals on their surface, due to their large surface area and surface hydrophobicity. The levels of contamination on the microplastic surface are significantly higher than in the natural environment. The gut-brain axis (GB axis), through which organisms interact with their environment, regulate nutritional digestion and absorption, intestinal motility and secretion, complex polysaccharide breakdown, and maintain intestinal integrity, can be altered by microplastics acting alone or in combination with pollutants. Probiotics have shown significant therapeutic potential in managing various illnesses mediated by the gut-brain axis. They connect hormonal and biochemical pathways to promote gut and brain health, making them a promising therapy option for a variety of GB axis-mediated illnesses. Additionally, taking probiotics with or without food can reduce the production of pro-inflammatory cytokines, reactive oxygen species (ROS), neuro-inflammation, neurodegeneration, protein folding, and both motor and non-motor symptoms in individuals with Parkinson's disease. This study provides new insight into microplastic-induced gut dysbiosis, its associated health risks, and the benefits of using both traditional and next-generation probiotics to maintain gut homeostasis.
ABSTRACT
Oxidative stress and the accumulation of misfolded proteins in the brain are the main causes of Parkinson's disease (PD). Several nanoparticles have been used as therapeutics for PD. Despite their therapeutic potential, these nanoparticles induce multiple stresses upon entry. Selenium (Se), an essential nutrient in the human body, helps in DNA formation, stress control, and cell protection from damage and infections. It can also regulate thyroid hormone metabolism, reduce brain damage, boost immunity, and promote reproductive health. Selenium nanoparticles (Se-NPs), a bioactive substance, have been employed as treatments in several disciplines, particularly as antioxidants. Se-NP, whether functionalized or not, can protect mitochondria by enhancing levels of reactive oxygen species (ROS) scavenging enzymes in the brain. They can also promote dopamine synthesis. By inhibiting the aggregation of tau, α-synuclein, and/or Aß, they can reduce the cellular toxicities. The ability of the blood-brain barrier to absorb Se-NPs which maintain a healthy microenvironment is essential for brain homeostasis. This review focuses on stress-induced neurodegeneration and its critical control using Se-NP. Due to its ability to inhibit cellular stress and the pathophysiologies of PD, Se-NP is a promising neuroprotector with its anti-inflammatory, non-toxic, and antimicrobial properties.
ABSTRACT
Microplastic (MP) tiny fragments (< 5 mm) of conventional and specialized industrial polymers are persistent and ubiquitous in both aquatic and terrestrial ecosystem. Breathing, ingestion, consumption of food stuffs, potable water, and skin are possible routes of MP exposure that pose potential human health risk. Various microorganisms including bacteria, cyanobacteria, and microalgae rapidly colonized on MP surfaces which initiate biofilm formation. It gradually changed the MP surface chemistry and polymer properties that attract environmental metals. Physicochemical and environmental parameters like polymer type, dissolved organic matter (DOM), pH, salinity, ion concentrations, and microbial community compositions regulate metal adsorption on MP biofilm surface. A set of highly conserved proteins tightly regulates metal uptake, subcellular distribution, storage, and transport to maintain cellular homeostasis. Exposure of metal-MP biofilm can disrupt that cellular homeostasis to induce toxicities. Imbalances in metal concentrations therefore led to neuronal network dysfunction, ROS, mitochondrial damage in diseases like Alzheimer's disease (AD), Parkinson's disease (PD), and Prion disorder. This review focuses on the biofilm development on MP surfaces, factors controlling the growth of MP biofilm which triggered metal accumulation to induce neurotoxicological consequences in human body and stategies to reestablish the homeostasis. Thus, the present study gives a new approach on the health risks of heavy metals associated with MP biofilm in which biofilms trigger metal accumulation and MPs serve as a vector for those accumulated metals causing metal dysbiosis in human body.
