How does arsenic affect rats? - briefly
Arsenic exposure in rats induces dose‑dependent toxicity, manifesting as weight loss, organ damage, and compromised neurological function. High concentrations cause mortality and severe histopathological alterations in liver, kidney, and brain.
How does arsenic affect rats? - in detail
Arsenic exposure in laboratory rats produces dose‑dependent toxicological outcomes that can be categorized into acute, sub‑chronic, and chronic effects.
In the acute phase (single doses exceeding 10 mg kg⁻¹), rats display rapid onset of gastrointestinal distress, respiratory depression, and central nervous system depression, often resulting in mortality within hours. Histopathological examination reveals hemorrhagic lesions in the stomach and duodenum, pulmonary edema, and necrosis of hepatic and renal parenchyma.
Sub‑chronic exposure (daily doses of 0.5–5 mg kg⁻¹ for 4–12 weeks) leads to measurable alterations in biochemical parameters. Blood analyses show elevated serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST), indicating hepatic injury; increased blood urea nitrogen (BUN) and creatinine, reflecting renal dysfunction; and reduced erythrocyte count, hemoglobin concentration, and hematocrit, consistent with anemia. Oxidative stress markers rise, with higher malondialdehyde (MDA) levels and depleted glutathione (GSH) in liver and brain tissues. Behavioral tests reveal impaired locomotor activity and decreased exploratory behavior, suggesting neurotoxicity.
Chronic ingestion (continuous exposure to 0.1–1 mg kg⁻¹ for 6 months or longer) produces progressive organ pathology. Liver sections demonstrate fibrosis, portal inflammation, and nodular regeneration. Kidneys exhibit tubular atrophy, interstitial fibrosis, and glomerular sclerosis. In the cardiovascular system, arterial walls thicken due to smooth‑muscle proliferation and collagen deposition, predisposing to hypertension. Reproductive organs are affected: male rats show reduced sperm count, motility, and altered morphology; females experience disrupted estrous cycles and decreased litter size. Carcinogenic potential is evident in increased incidence of hepatocellular adenomas and lung tumors in long‑term studies.
Mechanistically, arsenic interferes with cellular respiration by inhibiting pyruvate dehydrogenase and mitochondrial complex IV, leading to ATP depletion. It also impairs DNA repair enzymes, induces chromosomal aberrations, and activates signaling pathways (e.g., MAPK, NF‑κB) that promote inflammation and apoptosis. Epigenetic modifications, such as DNA methylation changes, have been documented in exposed rats, contributing to altered gene expression profiles.
Overall, arsenic toxicity in rats manifests as multi‑organ damage, oxidative stress, metabolic disruption, and carcinogenesis, with severity proportional to dose and exposure duration.