Microplastic sources, formation, toxicity and remediation: a review.

Microplastic pollution is becoming a major issue for human health due to the recent discovery of microplastics in most ecosystems. Here, we review the sources, formation, occurrence, toxicity and remediation methods of microplastics. We distinguish ocean-based and land-based sources of microplastics. Microplastics have been found in biological samples such as faeces, sputum, saliva, blood and placenta. Cancer, intestinal, pulmonary, cardiovascular, infectious and inflammatory diseases are induced or mediated by microplastics. Microplastic exposure during pregnancy and maternal period is also discussed. Remediation methods include coagulation, membrane bioreactors, sand filtration, adsorption, photocatalytic degradation, electrocoagulation and magnetic separation. Control strategies comprise reducing plastic usage, behavioural change, and using biodegradable plastics. Global plastic production has risen dramatically over the past 70 years to reach 359 million tonnes. China is the world's top producer, contributing 17.5% to global production, while Turkey generates the most plastic waste in the Mediterranean region, at 144 tonnes per day. Microplastics comprise 75% of marine waste, with land-based sources responsible for 80-90% of pollution, while ocean-based sources account for only 10-20%. Microplastics induce toxic effects on humans and animals, such as cytotoxicity, immune response, oxidative stress, barrier attributes, and genotoxicity, even at minimal dosages of 10 µg/mL. Ingestion of microplastics by marine animals results in alterations in gastrointestinal tract physiology, immune system depression, oxidative stress, cytotoxicity, differential gene expression, and growth inhibition. Furthermore, bioaccumulation of microplastics in the tissues of aquatic organisms can have adverse effects on the aquatic ecosystem, with potential transmission of microplastics to humans and birds. Changing individual behaviours and governmental actions, such as implementing bans, taxes, or pricing on plastic carrier bags, has significantly reduced plastic consumption to 8-85% in various countries worldwide. The microplastic minimisation approach follows an upside-down pyramid, starting with prevention, followed by reducing, reusing, recycling, recovering, and ending with disposal as the least preferable option.

The metabolic and molecular mechanisms of α­mangostin in cardiometabolic disorders (Review).

α­mangostin is a xanthone predominantly encountered in Garcinia mangostana. Extensive research has been carried out concerning the effects of this compound on various diseases, including obesity, cancer and metabolic disorders. The present review suggests that α­mangostin exerts promising anti­obesity, hepatoprotective, antidiabetic, cardioprotective, antioxidant and anti­inflammatory effects on various pathways in cardiometabolic diseases. The anti­obesity effects of α­mangostin include the reduction of body weight and adipose tissue size, the increase in fatty acid oxidation, the activation of hepatic AMP­activated protein kinase and Sirtuin­1, and the reduction of peroxisome proliferator­activated receptor γ expression. Hepatoprotective effects have been revealed, due to reduced fibrosis through transforming growth factor­ß 1 pathways, reduced apoptosis and steatosis through reduced sterol regulatory­element binding proteins expression. The antidiabetic effects include decreased fasting blood glucose levels, improved insulin sensitivity and the increased expression of GLUT transporters in various tissues. Cardioprotection is exhibited through the restoration of cardiac functions and structure, improved mitochondrial functions, the promotion of M2 macrophage populations, reduced endothelial and cardiomyocyte apoptosis and fibrosis, and reduced acid sphingomyelinase activity and ceramide depositions. The antioxidant effects of α­mangostin are mainly related to the modulation of antioxidant enzymes, the reduction of oxidative stress markers, the reduction of oxidative damage through a reduction in Sirtuin 3 expression mediated by phosphoinositide 3­kinase/protein kinase B/peroxisome proliferator­activated receptor­Î³ coactivator­1α signaling pathways, and to the increase in Nuclear factor­erythroid factor 2­related factor 2 and heme oxygenase­1 expression levels. The anti­inflammatory effects of α­mangostin include its modulation of nuclear factor­κB related pathways, the suppression of mitogen­activated protein kinase activation, increased macrophage polarization to M2, reduced inflammasome occurrence, increased Sirtuin 1 and 3 expression, the reduced expression of inducible nitric oxide synthase, the production of nitric oxide and prostaglandin E2, the reduced expression of Toll­like receptors and reduced proinflammatory cytokine levels. These effects demonstrate that α­mangostin may possess the properties required for a suitable candidate compound for the management of cardiometabolic diseases.