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Berberine, an alkaloid isolated from the plant Berberis aristata, has been found to inhibit significantly the carcinogenesis induced by 20-methylcholanthrene (200 microg/0.1 mL/mouse) or N-nitrosodiethylamine (NDEA; 0.02% NDEA in distilled water, 2.5 mL/animal by gavage, five days a week for 20 weeks) in a dose-dependent manner in small animals. Administration of berberine (0.5, 2.5 or 5.0 mg kg(-1)) could reduce significantly the incidence of tumour in animals after an injection of 20-methylcholanthrene and increased their life span compared with the control. When berberine (10, 25 or 50 mg kg(-1)) was administered simultaneously with NDEA, the markers of liver injury (liver weight, gamma-glutamyl transpeptidase activity and glutathione S-transferase level) were reduced significantly compared with animals treated with NDEA only, which resulted in all the values being elevated. A similar decrease was noted in the serum levels of lipid peroxide, bilirubin and glutamate pyruvate transaminase. Morphology of liver tissue and levels of marker enzymes indicated that berberine offered protection against chemical carcinogenesis.

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Gamma aminobutyric acid (GABA(A)) receptor functional status was analysed in partial hepatectomised (PH), lead nitrate (LN) induced hyperplastic and N-nitrosodiethylamine (NDEA) treated neoplastic rat livers during peak DNA synthesis. The high-affinity [3H]GABA binding significantly decreased in PH and NDEA rats and the receptor affinity decreased in NDEA and increased in LN rats compared with control. In NDEA, displacement analysis of [3H]GABA with muscimol showed loss of low-affinity site and a shift of high-affinity site towards low-affinity. The affinity sites shifted towards high-affinity in LN rats. The number of low-affinity [3H]bicuculline receptors decreased significantly in NDEA and PH whereas it increased in LN rats. GABA(A) receptor agonist, muscimol, dose dependently inhibited epidermal growth factor (EGF) induced DNA synthesis and enhanced the transforming growth factor beta1 (TGFbeta1) mediated DNA synthesis suppression in primary hepatocyte cultures. Our results suggest that GABA(A) receptor act as an inhibitory signal for hepatic cell proliferation.

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