Acute oral exposure to imidacloprid induces apoptosis and autophagy in the midgut of honey bee Apis mellifera workers

Abstract

The honey bee Apis mellifera is an important pollinator that increases the yield and quality of crops. In recent years, honey bee populations have declined in some parts of the world, which has been associated with several causes, including pesticides used in agriculture. Neonicotinoids are neurotoxic insecticides widely used in the world with systemic action mode contaminating nectar and pollen that may be consumed by bees. This study evaluated the side effects of imidacloprid in the midgut of A. mellifera after acute oral exposure. Toxicity, histopathology, cytotoxicity, and expression of autophagy-related gene atg1 were evaluated in honey bee workers orally exposed to imidacloprid. The estimated imidacloprid LC50 was 1.44 mg L−1. The midgut epithelium of bees fed on imidacloprid LC50 has the occurrence of cytoplasm vacuoles, enlarged intercellular spaces, disorganization of the striated border, and nuclear pyknosis, with an organ injury index that increases with time exposure. The midgut digestive cells of treated bees have apical protrusions, damaged mitochondria, and autophagosomes that were characterized for content with organelle debris and high expression of atg1. These features indicate the occurrence of high cell death in the midgut of workers exposed to imidacloprid, which may affect the digestibility the physiology of the insect.