How does boric acid affect mice? - briefly
Boric acid acts as a toxicant in rodents, impairing metabolic pathways and causing organ damage, weight loss, and death at doses exceeding approximately 200 mg kg⁻¹. Sublethal concentrations produce neurological effects, including tremors and reduced locomotor activity.
How does boric acid affect mice? - in detail
Boric acid (H₃BO₃) exhibits dose‑dependent toxicity in rodents, with measurable impacts on physiology, behavior, and organ integrity. Acute exposure at concentrations above 1 g kg⁻¹ body weight produces rapid respiratory distress, convulsions, and mortality. The median lethal dose (LD₅₀) for intraperitoneal administration in adult mice ranges from 1.5 to 2.0 g kg⁻¹, while oral LD₅₀ values are slightly higher, reflecting lower absorption through the gastrointestinal tract.
Sub‑lethal doses influence several biological systems:
- Neurological function: Low‑to‑moderate levels (0.1–0.5 g kg⁻¹) cause reduced locomotor activity, impaired coordination, and delayed reflexes, attributable to disruption of calcium signaling in neuronal cells.
- Reproductive health: Chronic ingestion of 0.05 g kg⁻¹ diet leads to decreased sperm count, altered estrous cycles, and reduced litter size, linked to endocrine interference and testicular degeneration.
- Renal and hepatic pathology: Histological examinations after 30 days of 0.2 g kg⁻¹ dietary exposure reveal tubular necrosis, glomerular congestion, and hepatocellular vacuolation, indicating organ toxicity mediated by oxidative stress.
- Immune response: Exposure at 0.01 g kg⁻¹ reduces splenic lymphocyte proliferation and suppresses antibody production, suggesting immunomodulatory effects.
Mechanistically, boric acid acts as a weak Lewis acid, forming complexes with diols and cis‑diols in biomolecules. This interaction perturbs enzyme activity, particularly those dependent on magnesium and calcium cofactors. Additionally, boric acid induces apoptosis through mitochondrial membrane depolarization and activation of caspase‑3 pathways.
Pharmacokinetic data show rapid absorption from the gastrointestinal tract, peak plasma concentrations within 1–2 hours, and primary excretion via urine. Tissue accumulation is modest, with the highest concentrations detected in the kidney and liver.
Experimental protocols commonly employ the following parameters:
- Route of administration: Oral gavage, intraperitoneal injection, or dietary incorporation.
- Dose range: 0.01–2.0 g kg⁻¹, adjusted for age, sex, and strain.
- Observation period: Acute studies last 24 hours; sub‑chronic designs extend to 90 days.
- Endpoints: Mortality, body‑weight change, behavioral scoring, serum biochemistry, and histopathology.
These findings support the classification of boric acid as a moderate toxicant for mice, with clear thresholds separating reversible functional alterations from irreversible organ damage and death. Proper dosing and exposure control are essential for experimental validity and animal welfare.