Mancozeb (MZ), a manganese‐ and zinc‐containing ethylene‐bis‐dithiocarbamate, is a broad‐spectrum fungicide. Harmful effects of this fungicide have been reported in nontarget organisms via a not fully understood mechanism. Drosophila melanogaster has provided remarkable contributions for toxicological studies. This work was aimed at evaluating the biochemical targets and implication of oxidative stress in MZ‐mediated toxicity in drosophilas. Exposure of flies for fifteen days to MZ at 5 and 10 mg/mL through the diet impaired locomotor performance and induced fly mortality. In parallel, it caused lipid peroxidation and reactive oxygen species (ROS) formation and Mn overload. MZ inhibited superoxide dismutase and inducted catalase and glutathione S‐transferase activities. Nitric oxide and reduced glutathione levels were significantly decreased by MZ. Heat shock proteins (HSP70 and HSP83) and Nrf2 mRNA levels were significantly augmented in MZ‐exposed flies. Our study reinforced the use of Drosophila melanogaster as a reliable model for the study of biochemical targets of pesticides, and based on our data, MZ induced oxidative damage and Mn accumulation in a concentration‐dependent manner. An adaptative cellular state was inducted by the lower concentration of pesticide, possibly contributing to the slighter damage observed.

Duguetia furfuracea is frequently used as a medicinal plant in Brazil. However, studies have evidenced its cytotoxic, bactericide, and antitumor activities. In the present study we aimed to evaluate the potential toxicity of hydroalcoholic leaves extracts of D. furfuracea (HEDF) in a Drosophila melanogaster model. Toxicity was assessed as changes in locomotor performance, mitochondrial activity, oxidative stress, MAPKs phosphorylation, and apoptosis induction after exposure to HEDF concentrations (1–50 mg/mL) for 7 days. The phytoconstituents of the plant were screened for the presence of alkaloids, tannins, xanthones, chalcones, flavonoids, aurones, and phenolic acids. Exposure of adult flies to HEDF caused mitochondrial dysfunction, overproduction of ROS, and alterations in the activity of detoxifying enzymes GST, SOD and CAT. Induction of ERK phosphorylation and PARP cleavage was also observed, indicating occurrence of HEDF‐induced cell stress and apoptotic cell death. In parallel, alterations in cholinesterase activity and impairments in negative geotaxis behavior were observed. Our study draws attention to the indiscriminate use of this plant by population and suggests oxidative stress as a major mechanism underlying its toxicity.

Fungal volatile organic compounds (VOCs) comprise a group of compounds commonly found in damp or water-damaged indoor places affecting air quality. Indoor fungal pollution is a severe threat to human health, contributing to the onset of allergic diseases. The compound 1-octen-3-ol, known as "mushroom alcohol", is the most abundant VOC and confers the characteristic mold odor. Exposure to 1-octen-3-ol induces inflammatory markers and episodes of allergic rhinitis and conjunctivitis; however, the effects of this compound towards mitochondria are fairly known. The present study aimed to evaluate the effects of 1-octen-3-ol on inflammatory targets and on mitochondrial morphology and bioenergetic rate in D. melanogaster. Drosophilas were exposed by inhalation to 2.5 μL/L and 5 μL/L of 1-octen-3-ol for 24 h. Observation showed a decreasing in the survival and locomotor ability of flies. Superoxide dismutase (SOD) activity was induced whereas Catalase (CAT) activity was inhibited. Analysis of the mitochondria respiration, detected inhibition of complex I and II in the electron transport chain and a decreased bioenergetic rate. Electronic microscopy provided morphological insights of the mitochondrial status in which a disarrangement in mitochondrial cristae profile was observed. 1-Octen-3-ol induced increased activity of caspase 3/7 and ERK phosphorylation. The mRNA relative steady-state levels of p38^MAPK and JNK were down-regulated, whereas NF-κB and p53 were up-regulated. In parallel, nitrite levels were induced in relation to the non-exposed group. These findings point to the mitochondria as a crucial target for the toxicity of 1-octen-3-ol in parallel with activation of pro-inflammatory factors and apoptotic signaling pathway cascade.