A review of food contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin and its toxicity associated with metabolic disorders.

Dioxins are a group of chemicals not only regarded as highly toxic trace environmental contaminants, but also considered typical contaminants in food. Dioxins spread across the ecosystem after factory manufacture, contaminate the soil and vegetation before either directly or indirectly entering the food chain through meat products, dairy products, and aquatic products. The compound in question poses a challenge for metabolic processes within the human body, due to its intricate mechanism for inducing diseases. Therefore, it presents a significant risk and is largely undisclosed. Dioxins are mainly exposed to humans by water, food, and air, as well as inducing organ failure and metabolic disorders through but not limited to the activation of aryl hydrocarbon receptors (AhR). As a notorious compound in the family of dioxins, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exhibits long-term toxic effects on diverse organs, which induces continuous metabolic disorders. This review discussed the mechanisms of TCDD-associated metabolic syndrome. The expression of the cytochrome P450 subfamily transfers TCDD into liver, promotes its accumulation in fat tissue, and affects cholesterol metabolism. This process also alters the glucose tolerance of the human organism, disrupting glucose metabolism. It can also elicit cardiovascular pathogenesis, exacerbate liver fibrosis and neuronal death. The long-term metabolic impact of this effect is found to be sex-related. This review summarized the toxicity of TCDD on the human metabolism system and discussed the plausible correlation between TCDD and five metabolic disorders, which helped offer novel insights for future research and therapeutic interventions for these ailments.