Effects of L-Carnitine on Aflatoxin B₁Toxicity

The effects of carnitine supplementation on AFB 1 toxicity in male Sprague-Dawley rats were studied. Rats were fed Purina Rat Chow with or without camitine supplement for 6 weeks. In Experiment 1, the rats (n=20) were divided into 4 groups, namely non-supplemented control (NSC), nonsupplemented AFB 1 (NSA), camitine supplemented control (CSC) and camitine supplemented AFBl (CSA) groups. The NSA and CSA groups were given an oral dose of [³H]AFB1 (1mg/kg) 6 h before sacrificing. In Experiment 2, the rats (n= 10) were divided into NSA and CSA groups and were sacrificed 24 h post-AFB 1 administration. Concentrations of total lipid, triglycerides, camitine and AFB I -macromolecules adduct formation, and urinary excretion of AFB 1 were measured. Carnitine supplementation prevented increase in hepatic total lipid and triglyceride concentrations caused by AFB 1. In the plasma, supplemental camitine prevented the AFB I-induced decrease in the amount of total lipid and triglyceride. Carnitine supplementation reduced AFB 1 covalent binding to hepatic macromolecules, namely RNA, DNA, and protein. The concentrations of RNA, DNA, and protein in the CSA rats were significantly higher than in the NSA animals 24 h post-AFB 1 treatment. [³H]AFB1 radioactivity was found in the acid insoluble acylcarnitine (AIAC) fraction. Carnitine supplement, however, had no significant effect on the amount of [³H]AFB 1 associated with AIAC. AFB 1 treatment of rats 6 h prior to sacrifice caused significant increase in the liver nonesterified camitine (NEC), acid soluble acylcarnitine (ASAC), and total carnitine. The amounts of AFB! in the liver, kidney and plasma were not significantly different in the NSA and CSA animals. The concentration of AFB 1 excreted in the urine was also not statistically different in the CSA and NSA rats. In conclusion, carnitine supplementation offered protection against AFB I-induced fatty liver and AFB I-macromolecule adducts formation.