Phthalates are the emerging environmental toxicants derived from phthalic acid and its constituents, which are moderately present in plastics and many personal care products. Phthalate exposure occurs through various environmental factors, including air, water, and soil, with absorption facilitated via ingestion, inhalation, and dermal contact. Upon exposure, phthalates become bioavailable within the biological systems and undergo biotransformation and detoxification processes in the liver. The physicochemical properties of phthalates indicate their lipophilicity, environmental persistence, and bioaccumulation potential, influencing their absorption, distribution, and hepatic biotransformation. The prolonged exposure to phthalates adversely influences the biological redox system by altering the levels of the enzymatic and non-enzymatic antioxidants, molecular signaling pathways, and causing hepatic pathogenesis. The strategies to combat phthalate-induced toxicity include avoiding exposure to these compounds and using plant-based bioactive molecules such as polyphenols, which possess therapeutic potential as antioxidants, suppress inflammatory cascades, prevent oxidative damage, and stabilize cellular integrity. This review presents a comprehensive and updated account of the chemical, biochemical, immunological, and toxicological properties of phthalates, along with novel plant-based therapeutic strategies to mitigate the phthalate-induced adverse effects on living systems.

Background: Arsenic (As), a poisonous metalloid, is widely distributed in air, water, and soil and has been associated with the occurrence of diabetes and liver toxicity. Zingerone (ZNG), one of the active compounds in ginger, has several pharmacological benefits such as antioxidant and anti-inflammatory characteristics. The objective of this research was to assess the protective role of ZNG against arsenic (As)-induced glucose intolerance (GI) and hepatotoxicity in mice. Methods: Male NMRI mice were treated with ZNG (25, 50, and 100 mg/kg, oral gavage for 29 days) before As administration (10 mg/kg, oral gavage for 29 days). On the 29th day, fasting blood glucose (FBG) and glucose tolerance test were measured. The animals were euthanized (day 30), and samples from blood and tissue (liver and pancreas) were gathered for further evaluations. Results: Administration of ZNG inhibited As-induced elevation of FBG and GI. Moreover, hepatic tissue damage and decreased Langerhans islets' diameter caused by As administration were improved by ZNG treatment. Pretreatment with ZNG attenuated the elevation of serum liver enzymes induced by As (alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase). Also, the reduction in total thiol content, as well as the decline in antioxidant enzyme activities (catalase, superoxide dismutase, and glutathione peroxidase) and the increase in lipid peroxidation marker (thiobarbituric acid reactive substances) in the liver tissue of Asexposed mice were reversed in ZNG-treated mice. Furthermore, ZNG prevented the increase of hepatic inflammatory markers (nitric oxide and tumor necrosis factor-alpha levels, and protein expression of nuclear factorkappa B) and apoptosis-related marker (caspase-3 protein expression) in As-treated mice. Conclusions: This study has provided evidence indicating that ZNG can act as a beneficial agent in preventing Asinduced hepatotoxicity and diabetes.