Cinnamomum cassia is used as a flavoring spice with some established medicinal properties. In this study, we evaluated the antimutagenic effect of C. cassia against two mutagens, viz. benzo[a]pyrene (B[a]P) and cyclophosphamide (CP). The antimutagenic properties of C. cassia were examined by the Ames test. In vivo chromosomal aberration (CA) and micronuclei tests were also employed to assess the antimutagenic effect of C. cassia in mice after pretreatment with the extract orally for seven consecutive days. To elucidate the mechanism by which C. cassia exerts its antimutagenic effect, certain key enzymes involved in bioactivation and detoxification processes were also investigated. Changes in liver cytochrome P450 (Cyt P450), glutathione content (GSH), glutathione S-transferase (GST), glutathione reductase (GR), and glutathione peroxidase (GPX) were evaluated in pretreated animals. It was observed in the Ames test, bone marrow chromosomal aberration assay, and micronucleus test that C. cassia exerted significant antimutagenic effects against B[a]P and CP in animals treated with the plant extract. C. cassia pretreatment decreased Cyt P450 content but increased GSH content and the activity of glutathione-dependent antioxidant enzymes, viz. GST, GR, and GPX. The present findings demonstrate that the antimutagenic potential of C. cassia could be attributed to its modulatory effect on the xenobiotic bioactivation and detoxification processes.

Inhibition of benzo[a]pyrene- and cyclophoshamide-induced mutagenicity by Cinnamomum cassia.

Benzo [α] pyrene (B[α]P) and cyclophosphamide (CP) are potent carcinogens/mutagens. Effect of Emblica officinalis extract administration on the in vivo genotoxi-city of B[α]P and CP was studied using bone marrow chromosomal aberration and micronucleus induction tests in mice.Three doses (50,250 and 500mg/kgbodyweight) oftheplant extractwere administered orallyfor 7 consecutive days prior to the administration of single dose of mutagens (B[α]P 125 mg/kg oral; CP 40 mg/kg i.p.).It was found that administration of 250 and 500 mg/kg of E. officinalis extract significantly inhibited the genotoxi-city of B [α] P as well as CP in both the assay systems. Administration of 50 mg/kg of the plant extract had no inhibitory effect.Vitamin C, a major constituent of E. officinalis when administered at dose level of 9 mg/kg b.w. (the approx-imate estimated amount present in the highest dose of plant extract, i.e. 500 mg) for 7 days did inhibit chromosomal aberrations and micronuclei induction, but not in a significant ma...

Inhibitory effect of Emblica officinalis on the in vivo clastogenicity of benzo[a]pyrene and cyclophosphamide in mice.

A method for evaluating pollutant genotoxicity, embryotoxicity and teratogenicity using sea urchin embryos has been developed and was tested using benzo(a)pyrene (BP). Initial results suggested that the bioassay may be a sensitive indicator of pollutant toxicity and mutagenicity since several endpoints can be simultaneously assessed. The bioassay is rapid, inexpensive and appears applicable to a variety of toxicants and delivery methods. The test is based upon the standard 48 h sea urchin development assay and incorporates cytologic-cytogenetic analysis of embryos. Following toxic exposure of gametes, fertilization success is assessed. Embryos then develop for 48 h at which time survival and teratogenesis are evaluated. A subsample of embryos is stained and dissociated into monolayers and mitotic configurations are examined using light microscopy. Embryo mitotic rates are used as an indicator of overall embryonic health. Cytotoxic effects are concomitantly evaluated. Genotoxicity is measured using two methods: (1) anaphase aberration analysis, a technique which assesses abnormalities in the chromosome configurations (such as bridges and fragments) as the groups of chromosomes move to opposite poles and (2) micronucleus formation, a procedure examining the incidence of smaller, secondary nuclei composed of whole chromosomes or chromatid fragments. These two measurements preclude the need to examine individual chromosomes for deletions and exchanges, a laborious process in most aquatic organisms which possess numerous relatively small chromosomes. This genotoxicity-teratogenicity test appears promising for laboratory evaluations of individual substances or of complex chemical mixtures as well as for environmental monitoring of nearshore areas. The standard development assay has been used to screen pharmaceuticals and environmental contaminants and some recent investigations have included mitotic aberration analysis. Experiments in our laboratory suggest that the genotoxicity-teratogenicity test may be a feasible approach to field monitoring. Mutagen loads of spawning adult urchins could be assessed by conducting cytologic-cytogenetic analysis of resulting embryos although initial studies suggest that this method is less sensitive than direct embryo exposures.

Potential uses of sea urchin embryos for identifying toxic chemicals: description of a bioassay incorporating cytologic, cytogenetic and embryologic endpoints.

Inhibition of in vivo genotoxicity by coffee

Inhibitory effects of coffee on the genotoxicity of carcinogens in mice

The effectiveness of 3 compounds, procarbazine, mitomycin C and cyclophosphamide as inducers of sister-chromatid exchanges (SCEs) in granulocyte-macrophage progenitor cells, in foetal liver and bone marrow from pregnant mice at day 17 of gestation were determined Cyclophosphamide and procarbazine induced similar SCE frquencies in maternal and foetal cells Mitomycin C was slightly less effective in foetal liver than in maternal bone marrow In contrast to the results of SCE induction, cyclophosphamide produced more micronucleated polychromatic erythrocytes in foetal liver than in bone marrow The SCE results for mitomycin C and procarbazine are compared with results obtained previously for micronuclei induction in 15-day pregnant animals

Z. Aghamohammadi

Papers

Sister-chromatid exchange and micronucleus induction as indicators of genetic damage in maternal and foetal cells.