Background: Arsenic is a ubiquitous metalloid in the environment and is extremely toxic to living systems. Low-dose sub chronic exposure alters cell metabolism, induces oxidative stress and damage to several organs. The aim of the present study was to quantify the histological biomarkers of arsenic toxicity in rats with a comprehensive morphopathological and quantitative approach.
Objectives: To characterise and quantify the histopathological changes in the liver, kidney and brain after graded doses of arsenite exposure in adult Wistar albino rats (Rattus norvegicus) and to derive indices of organ susceptibility for comparison based on structural and morphometric parameters.
Methods: Twenty-four adult male albino rats (Rattus norvegicus) were randomly divided into four groups (n = 6 each): control and three groups treated with sodium arsenite at doses 2, 4 and 8 mg/kg body weight/day by oral administration for 30 days. At the end of the exposure, the liver, kidney and brain tissues were excised, fixed in 10% neutral buffered formalin, and processed for histological evaluation by haematoxylin and eosin staining, PAS staining and Mallory’s trichrome staining. Lesions were scored semiquantitatively (0-3) and morphometric parameters were analysed by ImageJ software. Ordinal lesion scores and damage indices were analyzed using Kruskal–Wallis with Dunn’s test, while continuous variables were analyzed using ANOVA with Tukey’s test when assumptions were met (p < 0.05).
Results: All organs exhibited dose-dependent histopathological damage following arsenic exposure. The liver sections comprised vacuolar degeneration, sinusoidal dilation, and congestion. Renal tissues revealed tubular epithelial degeneration, glomerular atrophy and hyaline cast formation. Brain tissue showed neuronal vacuolation, necrosis and perivascular oedema. Morphometric investigation provided evidence for significant decreases in the diameter of hepatocytes and neurones and large increases in the width of sinusoids and perivascular spaces. Histological damage indices increased significantly with arsenic dose in all three organs, indicating substantial dose-dependent injury without a consistent fixed ranking of organ susceptibility across all exposure levels.
Conclusion: Arsenic induced dose dependent multisystem structural degeneration in rats following subchronic exposure. Sensitive quantitative measures of arsenic-induced organ injury and comparative assessment of organ susceptibility are provided by histopathological biomarkers and morphometric indices.