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Published on: February 22, 2016
Experimental acute arsenic toxicity in Balb/c mice: organic markers and splenic involvement
Alejandra Mariel Canalis1, Roberto Daniel Pérez2, Gisele Evangelina Falchini3
1Escuela de Nutrición, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Córdoba, Argentina; Consejo Nacional de Investigaciones Científicas y Técnicas, CONICET, Instituto de Investigaciones en Ciencias de la Salud, Córdoba, Argentina. canalisalejandra@hotmail.com.
Abstract:
Introduction: Arsenic is an environmental toxic present worldwide. In men and animals, various organs and tissues are targets of its deleterious effects including those of the immune system. Objective: To determine acute arsenic toxicity in tissues and target cells of Balb/c mice using an in vivo methodology. Materials and methods: We injected Balb/c mice intraperitoneally with 9.5 or 19 mg/kg of sodium arsenite (NaAsO2), or an equivalent volume of physiological solution as a control (with 3 per experimental group). After 30 minutes, the animals were sacrificed to obtain spleen, thymus, liver, kidneys, and blood. We determined arsenic, polyphenols, and iron concentrations in each sample and we evaluated the oxidative markers (peroxides, advanced products of protein oxidation, and free sulfhydryl groups). In splenocytes from the spleen, cell viability and mitochondrial potential were also determined. Results: The exposure to an acute dose of NaAsO2 reduced the mitochondrial function of splenocytes, which resulted in cell death. Simultaneously, the confirmed presence of arsenic in spleen samples and the resulting cytotoxicity occurred with a decrease in polyphenols, free sulfhydryl groups, and an alteration in the content and distribution of iron, but did not increase the production of peroxides. Conclusion: These findings provide scientific evidence about changes occurring in biomarkers involved in the immunotoxicity of arsenic and offer a methodology for testing possible treatments against the deleterious action of this compound on the immune system.
Insights
Acute arsenic exposure in mice damages immune cells by reducing mitochondrial function and causing cell death. This study identifies key biomarkers for arsenic immunotoxicity, aiding in the development of potential treatments.
Area of Science:
- Environmental Toxicology
- Immunology
- Biochemistry
Background:
- Arsenic is a widespread environmental toxicant with known deleterious effects on various organs and the immune system in humans and animals.
- Understanding the specific mechanisms of arsenic-induced immunotoxicity is crucial for public health and developing countermeasures.
Purpose of the Study:
- To investigate the acute toxicity of arsenic on immune tissues and cells in Balb/c mice using an in vivo model.
- To identify specific cellular and biochemical changes induced by acute arsenic exposure.
Main Methods:
- Balb/c mice were intraperitoneally injected with sodium arsenite (NaAsO2) at doses of 9.5 or 19 mg/kg.
- Tissues (spleen, thymus, liver, kidneys) and blood were collected 30 minutes post-injection for analysis.
- Arsenic, polyphenols, iron, and oxidative markers were quantified; splenocyte viability and mitochondrial potential were assessed.
Main Results:
- Acute sodium arsenite exposure reduced splenocyte mitochondrial function, leading to cell death.
- Arsenic presence in spleen samples correlated with decreased polyphenols and free sulfhydryl groups, and altered iron content.
- Oxidative markers, specifically peroxides, were not significantly increased by the acute arsenic dose.
Conclusions:
- This study provides evidence of arsenic-induced immunotoxicity, characterized by impaired mitochondrial function and cytotoxicity in immune cells.
- Alterations in polyphenols, sulfhydryl groups, and iron are identified as key biomarkers of arsenic's deleterious effects.
- The methodology presented can be used to evaluate potential treatments against arsenic toxicity.

