Toxicity Effect of Arsenic Trioxide on Hematological (RBC, WBC & Hemoglobin) and Morphological (Outside Body Reaction) Parameters in Mus musculus: A Comparative Study with Oral Administration of Control and Dose Groups

Abstract

Introduction

Background:

• Arsenic is a toxic metalloid found in water, soil, and industrial waste.

• Chronic exposure, especially to arsenic trioxide, causes oxidative stress, disrupting redox balance and damaging blood cells and tissues.

2. Objective:

To evaluate the dose-dependent toxicity of arsenic trioxide in mice by analyzing:

• Hematological parameters: RBC, WBC, hemoglobin

• Morphological and behavioral changes

• Histopathological effects

3. Methodology:

• Subjects: Adult Mus musculus (20–25g)

• Groups:

  • Control: Arsenic-free water

  • Low Dose: 1 mg/kg arsenic trioxide

  • High Dose: 3 mg/kg arsenic trioxide

• Duration: 60 days

• Analysis: Blood tests, behavioral observation, t-test for statistical analysis

4. Key Findings:

Hematological Effects:

• RBC Count: Decreased significantly in dose groups (High dose: 4.2 million/μL vs. Control: 8.2)

• WBC Count: Initial increase at low dose, then drop at high dose—indicating immune system stress and suppression

• Hemoglobin: Sharp decline, especially in high dose (7.8 g/dL vs. Control: 14.2)

Morphological and Behavioral Effects:

• Body Weight Loss: 25% reduction in high-dose group

• Fur Deterioration: Rough, discolored, patchy hair loss

• Behavior: Lethargy, reduced activity, stress signs

Histopathology:

• RBC apoptosis

• Suppressed bone marrow activity

• Damage in liver and spleen tissues

5. Statistical Results (t-Test):

• All comparisons between control and treated groups showed high statistical significance (p < 0.0001), confirming the dose-dependent toxic effects.

Conclusion

The findings from this study demonstrate a significant dose-dependent toxic effect of arsenic trioxide (As?O?) on both hematological and morphological parameters in Musmusculus. The comparative analysis between the control, low-dose, and high-dose groups reveals substantial physiological and behavioral alterations following arsenic exposure. A. Hematological Impact A pronounced decline in red blood cell (RBC) count and hemoglobin levels was observed in both arsenic-exposed groups. The high-dose group exhibited the most severe reduction, highlighting arsenic\'s direct cytotoxic effects on erythropoiesis and oxygen-carrying capacity. The decline in RBC count is indicative of hemolysis and impaired bone marrow function, aligning with known arsenic-induced oxidative stress and bone marrow suppression. White blood cell (WBC) count presented a biphasic response. In the low-dose group, an initial increase in WBC count suggests an acute immune response to arsenic-induced damage. However, in the high-dose group, the WBC count declined significantly, reflecting immune suppression and reduced hematopoietic activity. This immune suppression is consistent with arsenic\'s well-documented effects on immune cells and inflammatory pathways. B. Morphological and Behavioral Impact Body weight analysis revealed a dose-dependent reduction in arsenic-treated mice. The high-dose group exhibited severe weight loss, indicative of metabolic distress, reduced nutrient absorption, and organ dysfunction. This suggests arsenic\'s detrimental impact on systemic physiology and metabolic processes. Fur quality, evaluated on a scale from 0 to 10, deteriorated significantly in the arsenic-exposed groups. Mice in the high-dose group showed rough, patchy fur with visible hair loss, a classic sign of chronic toxicity and physiological stress. The control group maintained consistent fur quality, emphasizing the absence of adverse effects in arsenic-free conditions. Behavioral abnormalities, including lethargy and reduced movement, were evident in the high-dose group. These responses further suggest systemic toxicity, neurological impairment, and compromised well-being. C. Statistical Relevance The statistical analysis using the t-test confirmed the significance of these findings, with p-values below 0.05 for most comparisons between control and dose groups. The standard deviations and standard errors demonstrated the reliability of the data, reinforcing the validity of the observed dose-dependent trends. D. Final Remarks In summary, arsenic trioxide exposure leads to severe hematological alterations, including anemia and immune suppression, alongside marked morphological changes such as weight loss and fur deterioration. The results underscore arsenic\'s systemic toxicity and its potential to cause irreversible physiological damage. These findings emphasize the need for stringent regulations to minimize arsenic exposure in both occupational and environmental settings. Further research into mitigation strategies, detoxification approaches, and long-term effects is recommended to address the public health concerns associated with arsenic toxicity.

References

[1] Abernathy, C. O., et al. (2003). Health effects and risk assessment of arsenic. Journal of Nutrition, 133(5), 1536S-1538S. [2] Ahsan, H., et al. (2006). Arsenic exposure from drinking water and risk of premalignant skin lesions in Bangladesh. American Journal of Epidemiology, 163(6), 518-524. [3] Argos, M., et al. (2010). Arsenic exposure from drinking water and all-cause and chronic-disease mortalities in Bangladesh. The Lancet, 376(9737), 252-258. [4] Benbrahim-Tallaa, L., et al. (2013). Arsenic and cancer: Epidemiological and experimental evidence. Frontiers in Oncology, 3, 108. [5] Bergquist, E. R., et al. (2009). Arsenic detoxification by methylation and glutathione conjugation in mammals. Chemical Research in Toxicology, 22(10), 1711-1717. [6] [6.] Bhattacharya, P., et al. (2007). Arsenic in the environment: Biology and chemistry. Science of the Total Environment, 379(2-3), 109-120. [7] Bissen, M., &Frimmel, F. H. (2003). Arsenic: A review. Part I. Occurrence, toxicity, speciation, mobility. ActaHydrochimica et Hydrobiologica, 31(1), 9-18. [8] Buchet, J. P., et al. (1996). Assessment of exposure to inorganic arsenic and its metabolites in urine. Clinical Chemistry, 42(4), 588-595. [9] Chen, C. J., et al. (2004). Chronic arsenic exposure and health outcomes. Journal of Toxicology and Environmental Health, 67(5), 417-429. [10] Chen, Y., et al. (2007). Arsenic exposure from drinking water and mortality from cardiovascular disease in Bangladesh: Prospective cohort study. British Medical Journal, 334(7592), 173-176. [11] Chen, Z., et al. (2015). Arsenic-induced epigenetic changes and their role in carcinogenesis. Molecular and Cellular Biology, 35(16), 2790-2799. [12] Chiou, H. Y., et al. (2001). Arsenic methylation capacity and skin cancer risk in southwestern Taiwan. Journal of Environmental Health Perspectives, 109(9), 1011-1017. [13] Cullen, W. R., & Reimer, K. J. (1989). Arsenic speciation in the environment. Chemical Reviews, 89(4), 713-764. [14] Das, N., et al. (2016). Effect of arsenic toxicity on immune function. Environmental Toxicology and Pharmacology, 48, 60-70. [15] Dastgiri, S., et al. (2010). Arsenic exposure and hematological alterations: A systematic review. Journal of Environmental Health Science and Engineering, 7(2), 151-160. [16] Dopp, E., et al. (2004). Environmental arsenic toxicity, human exposure and carcinogenesis. Metal Ions in Biological Systems, 41, 321-339. [17] Dangleben, N. L., Skibola, C. F., & Smith, M. T. (2013). Arsenic immunotoxicity: A review. Environmental Health, 12(1), 73. [18] Farzan, S. F., et al. (2013). In utero arsenic exposure and infant morbidity: A prospective study in Bangladesh. Environmental Health Perspectives, 121(9), 1047-1052. [19] Flora, S. J. S. (2011). Arsenic-induced oxidative stress and its reversibility. Free Radical Biology and Medicine, 51(2), 257-281. [20] Ghosh, P., et al. (2007). Arsenic in groundwater and its effect on human health. Journal of Environmental Science and Health, Part A, 42(12), 1747-1754. [21] GuhaMazumder, D. N. (2008). Chronic arsenic toxicity: Clinical features and epidemiology. Indian Journal of Medical Research, 128(4), 436-447. [22] Hernández-Zavala, A., et al. (2009). Mechanisms of arsenic-induced carcinogenesis. Drug Metabolism Reviews, 41(2), 391-404. [23] Kitchin, K. T., &Conolly, R. (2010). Arsenic carcinogenesis. Environmental Health Perspectives, 118(7), 1104-1110. [24] Mandal, B. K., & Suzuki, K. T. (2002). Arsenic round the world: A review. Talanta, 58(1), 201-235. [25] Shen, S., et al. (2013). Arsenic binding and biomolecular interactions. Chemical Research in Toxicology, 26(7), 1122-1130. [26] Valko, M., Morris, H., & Cronin, M. T. (2005). Metals, toxicity, and oxidative stress. Current Medicinal Chemistry, 12(10), 1161-1208.

Copyright

Copyright © 2025 Sumit Kumar, Ashok Kumar Thakur. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.