Abstract
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.
Highlights
The use of plant extracts in the treatment and/or prevention of various diseases including cancer and cardiovascular diseases is recognized since ancient time, and some of these plants have led to the development of an impressive number of new drugs [1, 2]
Environmental stressors, toxic agents, and natural compounds as flavonoids [12,13,14] are reported to modulate the phosphorylation of mitogen activated protein kinases family (MAPKs), represented by ERK, c-Jun NH2-terminal kinase (JNK), and p38MAPK kinases, which participate in signaling pathways that are responsible for many cellular functions, such as growth, differentiation, and apoptosis
Our results demonstrated that 7 days of exposure of D. melanogaster to HEDF caused toxicity in a process involving oxidative stress, alterations in the antioxidant enzymes, MAPK proteins phosphorylation, and apoptotic cell death
Summary
The use of plant extracts in the treatment and/or prevention of various diseases including cancer and cardiovascular diseases is recognized since ancient time, and some of these plants have led to the development of an impressive number of new drugs [1, 2]. The growing use of plant extracts instead of synthetic compounds is primary because they are generally regarded as safe, accessible, affordable, and culturally acceptable form of health care trusted by large number of people [3,4,5,6]. Despite the beneficial effects of plant extracts, there are substantial evidences suggesting they can cause cytotoxicity [7, 8]. Evaluation of the toxic effects of plant extracts used in folk medicine seems to be imperative since they are generally consumed by population without concerns on their toxicity [9]. Oxidative stress, caused by overproduction of free radicals and/or alterations in antioxidant defense systems, is implicated as a mechanism of toxicity of many synthetic and natural compounds [10]. Environmental stressors, toxic agents, and natural compounds as flavonoids [12,13,14] are reported to modulate the phosphorylation of mitogen activated protein kinases family (MAPKs), represented by ERK, c-Jun NH2-terminal kinase (JNK), and p38MAPK kinases, which participate in signaling pathways that are responsible for many cellular functions, such as growth, differentiation, and apoptosis
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