Newly discovered developmental and ovarian toxicity of 3-monochloro-1,2-propanediol in Drosophila melanogaster and cyanidin-3-O-glucoside's protective effect

3-Monochloro-1,2-propanediol (3-MCPD) is a pervasive environmental pollutant that is unintentionally produced dur-ing industrial production and food processing. Although some studies reported the carcinogenicity and male reproduc-tion toxicity of 3-MCPD thus far, it remains unexplored whether 3-MCPD hazards to female fertility and long-term development. In this study, the model Drosophila melanogaster was employed to evaluate risk assessment of emerging environmental contaminants 3-MCPD at various levels. We found that flies on dietary exposure to 3-MCPD incurred lethality in a concentration-and time-dependent way and interfered with metamorphosis and ovarian development, resulting in developmental retardance, ovarian deformity and female fecundity disorders. Mechanistically, 3-MCPD caused redox imbalance observed as a drastically increased oxidative status in ovaries, confirmed by increased reactive oxygen species (ROS) and decreased antioxidant activities, which is probably responsible for female reproductive im-pairments and developmental retardance. Intriguingly, these defects can be substantially prevented by a natural anti-oxidant, cyanidin-3-O-glucoside (C3G), further confirming a critical role of ovarian oxidative damage in the developmental and reproductive toxicity of 3-MCPD. The present study expanded the findings that 3-MCPD acts as a developmental and female reproductive toxicant, and our work provides a theoretical basis for the exploitation of a natural antioxidant resource as a dietary antidote for the reproductive and developmental hazards of environmental toxicants that act via increasing ROS in the target organ.

Automated summary

This study evaluated the risk assessment of the emerging environmental pollutant 3-MCPD using the model organism Drosophila melanogaster. The results showed that dietary exposure to 3-MCPD caused lethality, interfered with metamorphosis and ovarian development, resulting in developmental retardance, ovarian deformity, and female fecundity disorders. Mechanistically, 3-MCPD induced redox imbalance in the ovaries, characterized by increased oxidative status and decreased antioxidant activities, which contributed to the reproductive impairments and developmental retardance.