Background:

Tritoqualine is used as a histidine decarboxylase inhibitor.

The effect of Tritoqualine (TRQ) on the CCl4-induced enzyme leakage is investigated by pretreatment of rats with Tritoqualine (200 mg/kg/day, p.o., 7 days). The ratio of lactate dehydrogenase (LDH) release from the cells of Tritoqualine-pretreated rats is significantly less than that in control rats. The rate of malondialdehyde (MDA) production is accelerated after the addition of 7.8 mM CCl4. Tritoqualine reduces its rate in a dose dependent manner, and it completely prevents CCl4-stimulated lipid peroxidation at a concentration of 33 μM[2].

A single administration of CCl4 (0.75 mL/kg, p.o.) causes a five-fold increase of in vivo lipid peroxidation in the liver. In contrast, a reduction of 37% in the lipid peroxidation is obtained by Tritoqualine (100 mg/kg) pretreatment for 14 days prior to CCl4 treatment. A 63% reduction is observed in vitamin E (25 mg/kg) pretreated rats[2].

[1]. Ishii K, et al. Therapeutic effect of histidine decarboxylase inhibitor on chronic active hepatitis. Gastroenterol Jpn. 1978;13(2):105-10. [2]. Yuasa S, et al. Suppressive effect of tritoqualine on lipid peroxidation and enzyme leakage induced by carbon tetrachloride in rat hepatocytes. Jpn J Pharmacol. 1986 Jun;41(2):205-10.