title: Low-Dose Aronia melanocarpa Concentrate Attenuates Paraquat-Induced Neurotoxicity.
abstract: Herbicides containing paraquat may contribute to the pathogenesis of neurodegenerative disorders such as Parkinson's disease. Paraquat induces reactive oxygen species-mediated apoptosis in neurons, which is a primary mechanism behind its toxicity. We sought to test the effectiveness of a commercially available polyphenol-rich Aronia melanocarpa (aronia berry) concentrate in the amelioration of paraquat-induced neurotoxicity. Considering the abundance of antioxidants in aronia berries, we hypothesized that aronia berry concentrate attenuates the paraquat-induced increase in reactive oxygen species and protects against paraquat-mediated neuronal cell death. Using a neuronal cell culture model, we observed that low doses of aronia berry concentrate protected against paraquat-mediated neurotoxicity. Additionally, low doses of the concentrate attenuated the paraquat-induced increase in superoxide, hydrogen peroxide, and oxidized glutathione levels. Interestingly, high doses of aronia berry concentrate increased neuronal superoxide levels independent of paraquat, while at the same time decreasing hydrogen peroxide. Moreover, high-dose aronia berry concentrate potentiated paraquat-induced superoxide production and neuronal cell death. In summary, aronia berry concentrate at low doses restores the homeostatic redox environment of neurons treated with paraquat, while high doses exacerbate the imbalance leading to further cell death. Our findings support that moderate levels of aronia berry concentrate may prevent reactive oxygen species-mediated neurotoxicity.
authors.affiliation: Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198-5850, USA.
authors.forename: A J
authors.initials: AJ
authors.lastname: Case
authors.affiliation: Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198-5850, USA.
authors.forename: D
authors.initials: D
authors.lastname: Agraz
authors.affiliation: College of Allied Health Professions, University of Nebraska Medical Center, Omaha, NE 68198, USA.
authors.forename: I M
authors.initials: IM
authors.lastname: Ahmad
authors.affiliation: Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198-5850, USA; Redox Biology Center, University of Nebraska Lincoln, Lincoln, NE 68588, USA.
authors.forename: M C
authors.initials: MC
authors.lastname: Zimmerman
mesh_terms: D000975:Antioxidants / Q000378:metabolism; D016923:Cell Death / Q000187:drug effects; D045744:Cell Line, Tumor; D004305:Dose-Response Relationship, Drug; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D009498:Neurotoxins / Q000633:toxicity*; D016877:Oxidants / Q000633:toxicity; D010084:Oxidation-Reduction / Q000187:drug effects; D010269:Paraquat / Q000633:toxicity*; D046936:Photinia / Q000737:chemistry*; D010936:Plant Extracts / Q000494:pharmacology*; D013481:Superoxides / Q000378:metabolism
chemical_list: D000975:Antioxidants; D009498:Neurotoxins; D016877:Oxidants; D010936:Plant Extracts; D013481:Superoxides; D006861:Hydrogen Peroxide; D005978:Glutathione; D010269:Paraquat