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.

Anthocyanins are mainly purple-coloured phenolic compounds of plant origin that as secondary metabolites are important in plant survival. Understanding their health benefits in humans requires sourcing these unstable compounds in sufficient quantities at a reasonable cost, which has led to improved methods of extraction. Dark-coloured fruits, cereals and vegetables are current sources of these compounds. The range of potential sustainable sources is much larger and includes non-commercialised native plants from around the world and agri-waste containing anthocyanins. In the last 5 years, there have been significant advances in developing the therapeutic potential of anthocyanins in chronic human diseases. Anthocyanins exert their beneficial effects through improvements in gut microbiota, oxidative stress and inflammation, and modulation of neuropeptides such as insulin-like growth factor-1. Their health benefits in humans include reduced cognitive decline; protection of organs such as the liver, as well as the cardiovascular system, gastrointestinal tract and kidneys; improvements in bone health and obesity; and regulation of glucose and lipid metabolism. This review summarises some of the sources of anthocyanins and their mechanisms and benefits in the treatment of chronic human diseases.

α‑mangostin 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 α‑mangostin exerts promising anti‑obesity, hepatoprotective, antidiabetic, cardioprotective, antioxidant and anti‑inflammatory effects on various pathways in cardiometabolic diseases. The anti‑obesity effects of α‑mangostin include the reduction of body weight and adipose tissue size, the increase in fatty acid oxidation, the activation of hepatic AMP‑activated protein kinase and Sirtuin‑1, and the reduction of peroxisome proliferator‑activated receptor γ expression. Hepatoprotective effects have been revealed, due to reduced fibrosis through transforming growth factor‑β 1 pathways, reduced apoptosis and steatosis through reduced sterol regulatory‑element 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 α‑mangostin 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 3‑kinase/protein kinase B/peroxisome proliferator‑activated receptor‑γ coactivator‑1α signaling pathways, and to the increase in Nuclear factor‑erythroid factor 2‑related factor 2 and heme oxygenase‑1 expression levels. The anti‑inflammatory effects of α‑mangostin include its modulation of nuclear factor‑κB related pathways, the suppression of mitogen‑activated 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 Toll‑like receptors and reduced proinflammatory cytokine levels. These effects demonstrate that α‑mangostin may possess the properties required for a suitable candidate compound for the management of cardiometabolic diseases.

The pulp of the purple mangosteen, Garcinia mangostana, is a popular tropical fruit but the rind containing xanthones such as α-mangostin together with procyanidins and anthocyanidins is usually discarded as waste. However, this rind has been used in South-East Asia for diarrhoea, dysentery, skin infections and wounds. As xanthones have reported anti-inflammatory and antioxidant responses, this study has determined the bioactive compounds and evaluated the effects of G. mangostana rind on physiological, metabolic, liver and cardiovascular parameters in rats with diet-induced metabolic syndrome. Rats fed a diet with increased simple sugars and saturated fats developed obesity, hypertension, increased left ventricular stiffness, dyslipidaemia and fatty liver. Administration of G. mangostana rind as 5% of the food to rats with diet-induced metabolic syndrome gave a dose of 168 mg/kg/day α-mangostin, 355 mg/kg/day procyanidins, 3.9 mg/kg/day anthocyanins and 11.8 mg/kg/day hydroxycitric acid for 8 weeks which reduced body weight and attenuated physiological and metabolic changes in rats including decreased abdominal fat deposition, decreased abdominal circumference and whole-body fat mass, improved liver structure and function and improved cardiovascular parameters such as systolic blood pressure, left ventricular stiffness and endothelial function. These responses were associated with decreased infiltration of inflammatory cells, decreased deposition of collagen in both heart and liver and decreased mean adipocyte size in retroperitoneal adipose tissues. We conclude that, in rats with diet-induced metabolic syndrome, chronic intake of G. mangostana rind decreased infiltration of inflammatory cells which decreased physiological, metabolic, liver and cardiovascular symptoms.