Oral exposure to inorganic mercury or methylmercury elicits distinct pro-inflammatory and pro-oxidant intestinal responses in a mouse model system

Rodríguez-Viso, Pilar; Domene, Adrián; Vélez, Dinoraz; Devesa, Vicenta; Monedero, Vicente; Zúñiga, Manuel

doi:10.1016/j.fct.2023.113801

Cited by 5 publications

(1 citation statement)

References 41 publications

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“…Over the last decade, evidence has accumulated for the role of reactive oxygen metabolites as a mediator of tissue injury in several animal models [16]. The pro-oxidant properties of Hg have been documented over time [17]. Concerning the mechanism, research supports the view that Hg (II) ions both compromise the antioxidant potential of glutathione and promote the formation of reactive species through thiol complexation.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the Potential Protective Effect of Ellagic Acid against Heavy Metal (Cadmium, Mercury, and Lead) Toxicity in SH-SY5Y Neuroblastoma Cells

Mallamaci,

Barbarossa,

Carocci

et al. 2024

Foods

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Ellagic acid (EA), a polyphenolic constituent of plant origin, has been thoroughly investigated for its hypothesised pharmacological properties among which antioxidant and neuroprotective activities are included. The present study was designed to explore whether EA could attenuate heavy metal (cadmium, mercury, and lead)-induced neurotoxicity in SH-SY5Y cells, which were utilized as a model system for brain cells. MTT and LDH assays were performed to examine the viability of the SH-SY5Y cells after exposure to Cd, Hg, and Pb (either individually or in combination with EA) as well as the effects of necrotic cell death, respectively. Furthermore, 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA), a cell-based assay, was performed to determine whether EA could protect SH-SY5Y from heavy metal-induced oxidative stress. Results allowed us to assess the capability of EA to enhance the number of viable SH-SY5Y cells after exposure to heavy metal toxicity. Pre-treatment with EA showed a considerable, concentration-dependent, cytoprotective effect, particularly against Cd2+-induced toxicity. This effect was confirmed through the reduction of LDH release after the simultaneous cell treatment with Cd2+ and EA compared with Cd2+-treated cells. Furthermore, a significant, concentration-dependent decrease in reactive oxygen species (ROS) production, induced by H2O2 or heavy metals, was observed in the same model. Overall, the obtained results provide further insight into the protective role of EA against heavy metal-induced neurotoxicity and oxidative stress, thus indicating the potential beneficial effects of the consumption of EA-rich foods. However, to confirm its effects, well-designed human randomized controlled trials are needed to fill the existing gap between experimental and clinical research.

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Section: Introductionmentioning

confidence: 99%