Acute exposure of mercury chloride stimulates the tissue regeneration program and reactive oxygen species production in the Drosophila midgut

• Mercury was largely sequestered within the midgut epithelia of Drosophila after oral administration.
• Mercury stimulation induced excess production of reactive oxygen species in the midgut epithelia.
• Mercury stimulation caused increased cell death.
• Mercury stimulation triggered tissue regeneration through accelerated proliferation and differentiation of intestinal stem cells.
• Vitamin E efficiently alleviated the HgCl2-induced tissue damages and improved the survival rate.

We used Drosophila as an animal model to study the digestive tract in response to the exposure of inorganic mercury (HgCl2). We found that after oral administration, mercury was mainly sequestered within the midgut. This resulted in increased cell death, which in turn stimulated the tissue regeneration program, including accelerated proliferation and differentiation of the intestinal stem cells (ISCs). We further demonstrated that these injuries correlate closely with the excessive production of the reactive oxygen species (ROS), as vitamin E, an antioxidant reagent, efficiently suppressed the HgCl2-induced phenotypes of midgut and improved the viability. We propose that the Drosophila midgut could serve as a suitable model to study the treatment of acute hydrargyrism on the digestive systems.