Effects of the insecticide imidacloprid on the post-embryonic development of the honey bee Apis mellifera (Hymenoptera: Apidae).

The widespread use of pesticides in agriculture has been linked to declines in bee populations worldwide. Imidacloprid is a widely used systemic insecticide that can be found in the pollen and nectar of plants and has the potential to negatively impact the development of bee larvae. We investigated the effects of oral exposure to a realistic field concentration (20.5 ng g-1) of imidacloprid on the midgut and fat body of Apis mellifera worker larvae. Our results showed that larvae exposed to imidacloprid exhibited changes in the midgut epithelium, including disorganization of the brush border, nuclear chromatin condensation, cytoplasm vacuolization, and release of cell fragments indication cell death. Additionally, histochemical analysis revealed that the midgut brush border glycocalyx was disorganized in exposed larvae. The fat body cells of imidacloprid-exposed larvae had a decrease in the size of lipid droplets from 50 to 8 µm and increase of 100 % of protein content, suggesting possible responses to the stress caused by the insecticide. However, the expression of de cdc20 gene, which plays a role in cell proliferation, was not affected in the midgut and fat body of treated larvae. These results suggest that imidacloprid negatively affects non-target organs during the larval development of A. mellifera potentially impacting this important pollinator species.

The fungicide azoxystrobin causes histopathological and cytotoxic changes in the midgut of the honey bee Apis mellifera (Hymenoptera: Apidae).

Apis mellifera is an important bee pollinating native and crop plants but its recent population decline has been linked to the use of pesticides, including fungicides that have been commonly classified as safe for bees. However, many pesticides, in addition to direct mortality cause sublethal effects, including damage to target selective honey bee organs. The midgut is the organ responsible for the digestion and absorption of nutrients and the detoxification of ingested substances, such as pesticides. This study evaluated the histopathological and cytotoxic changes in the midgut of A. mellifera workers caused by the pesticide azoxystrobin. The limit-test was performed, and a 100 µg a.i./bee dose was administered orally and midgut analyzed with light and transmission electron microscopies after 24 h and 48 h of pesticide exposure. The midgut of the control bees has a single layer of digestive cells, with spherical nuclei, nests of regenerative cells, and the lumen coated with the peritrophic matrix. The bees fed on azoxystrobin showed morphological changes, including intense cytoplasm vacuolization and cell fragments released into the gut lumen. The protein detection test showed greater staining intensity in the nests of regenerative cells after 24 h of exposure to azoxystrobin. The occurrence of damage to the midgut in A. mellifera exposed to azoxystrobin indicates that although this fungicide has been classified as low toxicity for bees, it has sublethal effects in the midgut, and effects in other organs should be investigated.

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

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.

Spiromesifen induces histopathological and cytotoxic changes in the midgut of the honeybee Apis mellifera (Hymenoptera: Apidae).

The honeybee Apis mellifera is an important pollinator that, similarly to other bees, undergoes colony losses due to several problems, including the use of pesticides in the agriculture. In addition to direct mortality, pesticides cause side-effects in some non-target organs, such as the midgut, which is the main organ for digestion and absorption. Spiromesifen is a pesticide used to control mites and whiteflies, which can be ingested by bees feeding on contaminated floral resources. This study evaluated the histopathological and cytological effects of the ingestion of spiromesifen on the midgut of A. mellifera workers. The bees were exposed per os to the field recommended dose of spiromesifen, and the midgut was analyzed after 24h and 48h of exposure to the pesticide. The midgut has a single layer of digestive cells, with spherical nucleus, nests of regenerative cells and layers of peritrophic matrix in the lumen. Bees treated with spiromesifen presented histological and cytological changes in the midgut, including disorganization of the epithelial architecture, release of cell fragments to the lumen, accumulation of mitochondria in the apical cytoplasm, alteration of the basal labyrinth, changes in the rough endoplasmic reticulum and cell degeneration. The occurrence of damage in the digestive cells of the A. mellifera midgut indicates that spiromesifen does not cause mortality in honeybees, but its side-effects can damage the midgut, which may affect the longevity and behavior of this pollinator.