Changes in hypopharyngeal glands of nurse bees (Apis mellifera) induced by pollen-containing sublethal doses of the herbicide Roundup®.

Decreasing pollinator populations worldwide has generated great concern and stimulated countless studies to understand the origin of colony losses. One main cause is the indiscriminate use of different pesticides, producing subtle negative effects on bee physiology and behavior. Royal jelly synthesized in the hypopharyngeal glands is an essential protein for feeding all individuals of the hive, especially the queen. Therefore, the present study aimed to determine the effect of sublethal concentrations of Roundup® on the hypopharyngeal glands of nursing workers, including its interference with the production of royal jelly. The herbicide was found to promote changes in the cellular ultrastructure of these glands, causing early degeneration of the rough endoplasmic reticulum and morphological and structural changes in the mitochondria. No changes were noted in the amount of royal jelly produced, but additional long-term studies are necessary to determine possible qualitative changes. This is the first study to evaluate the effect of Roundup® on the royal jelly-producing glands, showing that resultant alterations in these structures can trigger damage to the development and survival of bee colonies.

Diphenyl diselenide administration enhances cortical mitochondrial number and activity by increasing hemeoxygenase type 1 content in a methylmercury-induced neurotoxicity mouse model.

Interest in biochemistry of organoselenium compound has increased in the last decades, mainly due to their chemical and biological activities. Here, we investigated the protective effect of diphenyl diselenide (PhSe)2 (5 µmol/kg), in a mouse model of methylmercury (MeHg)-induced brain toxicity. Swiss male mice were divided into four experimental groups: control, (PhSe)2 (5 µmol/kg, subcutaneous administration), MeHg (40 mg/L, in tap water), and MeHg + (PhSe)2. After the treatment (21 days), the animals were killed and the cerebral cortex was analyzed. Electron microscopy indicated an enlarged and fused mitochondria leading to a reduced number of organelles, in the MeHg-exposed mice. Furthermore, cortical creatine kinase activity, a sensitive mitochondrial oxidative stress sensor, was almost abolished by MeHg. Subcutaneous (PhSe)2 co-treatment rescued from MeHg-induced mitochondrial alterations. (PhSe)2 also behaved as an enhancer of mitochondrial biogenesis, by increasing cortical mitochondria content in mouse-receiving (PhSe)2 alone. Mechanistically, (PhSe)2 (1 µM; 24 h) would trigger the cytoprotective Nrf-2 pathway for activating target genes, since astroglial cells exposed to the chalcogen showed increased content of hemeoxygenase type 1, a sensitive marker of the activation of this via. Thus, it is proposed that the (PhSe)2-neuroprotective effect might be linked to its mitoprotective activity.