Eryngium creticum L., Nigella sativa L., and Teucrium polium L. have been traditionally used for the treatment of inflammations, liver disorders,
and arthritis.
Several studies on these plants revealed antioxidant, anti-inflammatory, hepatoprotective,
antimutagenic and antiulcerogenic activities. In this study the antimutagenic activity
of these plant species was tested in rat hepatocyte primary cultures by treatment
with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), a directly acting mutagen, which was shown to induce massive
chromosomal damage in hepatocytes [1].
Since it cannot be excluded that the active constituents of the plant extracts require
biotransformation or induce metabolic enzymes, causing antimutagenic or detoxifying
effects, the present investigation was carried out with metabolically competent primary
cultures of rat hepatocytes.
Rat hepatocytes were isolated as described by Michalopoulos et al. [2]. Establishment of primary cultures and cytogenetic studies were performed according
to Eckl et al. [1].
Plant extracts were prepared by Soxhlet continuous extraction method, 6 gm of ground
plant materials were extracted in 50 mL of absolute ethanol at 85°C for 20 hours,
ethanol was air dried and the remaining oily extracts were dissolved in 5 mL of dimethyl
sulfoxide (DMSO).
Antimutagenicity testing was done in three modes: pre-treatment, combined treatment
and post-treatment of the primary cultures with plant extracts and MNNG. Therefore,
both the induction of metabolizing enzymes, direct interaction of plant constituents
with the mutagen and increased recovery, i.e. enhanced repair of induced DNA damage
can be evaluated. Student's double sided t-test for independent samples was used to
evaluate the levels of significance.
The results of our investigation clearly indicate an inhibitory effect on MNNG mutagenicity
by the three plant extracts, and this effect can be attributed to a direct antimutagenic
activity and an increased recovery.
Acknowledgments: This investigation was supported by a stipend of the Austrian Exchange Service (OEAD).
References: 1. Eckl, P.M. et al. (1987), Carcenogenisis 8:1077–1083. 2. Michalopoulos, G. et al. (1982), Cancer Res. 42:4673–4682.