Evaluating the protective effects of choline chloride on biochemical alterations induced by paracetamol toxicity in mice: A pilot study

Paracetamol (acetaminophen, APAP) toxicity is a significant clinical concern due to its hepatotoxic and nephrotoxic effects, which can lead to disruptions in serum protein synthesis, metabolic changes, and electrolyte imbalances. This study aimed to investigate the biochemical impacts of paracetamol toxicity and evaluate the potential protective effects of choline chloride. Using an in vivo model with balb/c mice, three groups were examined: A control group, an APAP-toxicity group (300 mg/kg paracetamol), and a choline-treated group (300 mg/kg paracetamol with 30 mg/kg choline chloride). Biochemical analyses revealed that paracetamol administration caused a slight but non-significant decrease in serum total protein and albumin levels, reflecting impaired hepatic function. While the toxicity model also showed significant reductions in glucose and triglyceride levels, cholesterol and electrolyte changes were non-significant. Notably, treatment with choline chloride led to a significant increase in serum potassium levels but did not significantly alter other biochemical markers within 24 h. These findings suggest that while choline chloride may support electrolyte balance and modulate certain metabolic disruptions, the short-term model may not capture long-term or more profound biochemical alterations. The study underscores the importance of further research to explore the protective role of choline and extended observation periods to better understand paracetamol-induced toxicity and recovery mechanisms.