Systemic toxicity is increasingly recognized as a coordinated biochemical disturbance involving multiple organ systems rather than isolated organ injury. This study investigated sodium fluoride (NaF)–induced multisystem biochemical toxicity in experimental rats through an integrated assessment of hepatic, renal, lipid, electrolyte, and oxidative stress indices. Twenty-one adult male rats were randomly assigned to seven experimental groups (n = 3 per group). Oxidative stress was induced by oral administration of NaF at graded doses of 5, 10, and 20 mg/kg body weight once daily for 28 consecutive days, while control animals received the appropriate vehicle. Serum biochemical parameters were analysed using standard spectrophotometric and enzymatic methods, and data were evaluated using one-way analysis of variance with appropriate post-hoc testing.
NaF exposure resulted in significant elevations in hepatic enzymes and bilirubin fractions, accompanied by reductions in plasma protein levels, indicating impaired hepatocellular integrity and synthetic function. Renal dysfunction was evidenced by marked increases in serum urea and creatinine levels, together with pronounced electrolyte imbalance. Significant alterations in lipid profile parameters, characterised by elevated total cholesterol and triglyceride levels with reduced high-density lipoprotein concentrations, indicated disruption of lipid metabolism. Antioxidant enzyme activities were significantly reduced, while malondialdehyde levels were markedly elevated, confirming enhanced oxidative stress.
In conclusion, sodium fluoride exposure induces widespread biochemical disruption involving hepatic, renal, metabolic, and redox pathways. These findings highlight oxidative stress as a central mediator of multisystem toxicity and underscore the importance of integrated biochemical assessment for comprehensive toxicological risk evaluation.