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The present work was conducted to evaluate the genotoxic effect of carbon tetrachloride (CCl) in mouse bone marrow and male germ cells. The safety and the modulating activity of sage (Salvia officinalis L.) essential oil (SEO) against the possible genotoxic effect of CCl were also evaluated. A combination of in vivo mutagenic endpoints was included: micronucleus (MN), apoptosis using dual acridine orange/ethidium bromide (AO/EB) staining, comet assay, chromosomal aberrations (CAs), and sperm abnormalities. Histological examination of testis tissues was also studied. The extracted SEO was subjected to gas chromatography-mass spectrometry (GC-MS) for identifying its chemical constituents. Safety/genotoxicity of SEO was determined after two consecutive weeks (5 days/week) from oral treatment with different concentrations (0.1, 0.2, and 0.4 mL/kg). For assessing genotoxicity of CCl, both acute (once) and subacute i.p. treatment for 2 weeks (3 days/week) with the concentrations 1.2 mL/kg (for acute) and 0.8 mL/kg (for subacute) were performed. For evaluating the protective role of SEO, simultaneous treatment with SEO plus CCl was examined. In sperm abnormalities, mice were treated with the subject materials for five successive days and the samples were collected after 35 days from the beginning of treatment. Based on GC-MS findings, 22 components were identified in the chromatogram of SEO. The results demonstrated that the three concentrations of SEO were safe and non-genotoxic in all the tested endpoints. Negative results were also observed in bone marrow after acute and subacute treatment with CCl In contrast, CCl induced testicular DNA damage as evidenced by a significant increase of CAs in primary spermatocytes, sperm abnormalities, and histological distortion of testis. A remarkable reduction in these cells was observed in groups treated with SEO plus CCl especially with the two higher concentrations of SEO. In conclusion, SEO is safe and non-genotoxic under the tested conditions and can modulate genetic damage and histological alteration induced by CCl in the testes.

The genotoxic effect of cadmium chloride was evaluated in chromosomes of experimental mice using in vivo and in vitro studies. In vivo the induction of micronuclei, sister chromatid exchange in mouse bone marrow and chromosomal aberrations in both somatic and germ cells was investigated. Doses 1.9, 5.7 and 7.6 mg kg ؊1 body wt. (single i.p. treatment) induced a significant and dose-dependent increase in the percentage of polychromatic erythrocytes with micronuclei. Such a percentage reached 2.1% with the highest tested dose, compared with 0.57% for the control (non-treated) and 2.2% for mitomycin c as the positive control. The dose of 1.9 mg kg ؊1 body wt. had no significant effect with respect to sister chromatid exchange (SCE) but the doses of 5.7 and 7.6 mg kg ؊1 body wt. increased the frequency of SCEs significantly. The frequency of SCE reached 7.35 ؎ 0.26 per cell after treatment with the highest tested dose, which is a less than twofold increase compared with the control frequency of 4.6 ؎ 0.42 per cell. However mitomycin c induced a much higher effect (12.1 ؎ 0.73). Cadmium chloride also induced a significant increase in the percentage of chromosomal aberrations in mouse bone marrow at the doses of 5.7 and 9.5 mg kg ؊1 body wt. (single i.p. treatment). The effect is a function of cadmium chloride concentration. Moreover, cadmium chloride induced its maximum effect concerning the induction of chromosomal aberrations in mouse bone marrow cells 24 h after treatment, compared with 12 and 48 h.In germ cells, chromosomal aberrations were observed in mouse spermatocytes 12 days post-treatment with the dose of 5.7 mg kg ؊1 body wt. Moreover, a pronounced reduction in the number of spermatocytes was observed after administration of cadmium chloride (0.9, 1.9 and 5.7 mg kg ؊1 body wt.)In in vitro studies, the three tested concentrations of 10, 15 and 20 g ml ؊1 cadmium chloride induced a statistically significant increase in the frequency of SCEs in cultured mouse spleen cells. The concentrations of 15 and 20 g ml ؊1 also induced chromosomal aberrations in mouse spleen culture.The ability of vitamin C (l-ascorbic acid) to minimize the incidence of chromosomal aberrations induced by cadmium chloride in cultured mouse spleen cells was investigated. Vitamin C at the concentrations of 3 and 6 g ml ؊1 significantly minimized the percentage of aberrant cells induced by cadmium chloride. P Ͻ 0.05 level; **significant at P Ͻ 0.01 level (t-test).

The present research designed to assess the protective role of Salvia officinalis essential oil (SO) against carbon tetrachloride (CCl)-induced liver and kidney damage in mice. This is evidenced by estimation of antiradical scavenging activity of SO using DPPH assay, biochemical markers, histological investigation of liver and kidney sections, and comet assay. Mice were given CCl (1.2 mL/kg for 24 h or 0.8 mL/kg for 2 weeks, 3 times/week) and with or without SO (0.1, 0.2, and 0.4 mL/kg, for 2 week, 5 times/week). The findings demonstrated that both acute and subacute treatment with CCl alone had adverse side effects on liver and kidney of mice. These effects were evidenced by a significant increase in serum hepatic enzymes (ALT, AST, ALP, LDH, and G-GT), bilirubin, and renal function markers (blood urea, creatinine). Toxic effect of CCl was accompanied by a decline in the serum total protein, albumin, globulin, and prothrombin (%). CCl induced oxidative stress as evidenced by increasing serum lipid peroxidation (LPO) along with decreasing serum total glutathione S transferase (GST). A remarkable increase in hepatic DNA strand breakages and histopathological distortion in liver and kidney specimens were observed in CCl-intoxicated groups. Ultrastructurally, hepatocytes exhibited irregular nuclei, vacuolated cytoplasm, and distorted microorganelles. Essential oil form S. officinalis possessed antiradical scavenging (EC = 4602 μg/mL) lower than ascorbic acid (EC = 5.9 μg/mL). This oil was effectively exhibited hepato-nephroprotective activity especially at its higher concentrations in co-treated groups (SO plus CCl). The activity of SO was associated with lowering the liver enzymes, bilirubin, urea, and creatinine, along with increasing total protein, albumin, globulin, and prothrombin. The increase in GST content and the decrease in LPO and DNA breakage levels, alongside repairing the histo-architectural distortions further confirmed the protective activity of SO. SO is a potential candidate for counteracting hepato/renal injury associating CCl. This effect may occur via antioxidant defense mechanism which in part related to the complexity of its chemical constituents.

SummaryThe genotoxic effects of cobalt chloride (CoCl 2 ) were studied in mice using different mutagenic end points in vivo. The possible protection provided by the antioxidant selenium and vitamins (ACE) against CoCl 2 genotoxicity was also assessed. The results indicate that CoCl 2 has genotoxic effects on mice somatic and germ cells. It induced a significant increase in the frequency of chromosomal aberrations in mouse bone-marrow and spermatocytes after single and repeated oral treatments. The induction of morphological sperm abnormalities was also confirmed in the present study. The supplemental selenium and vitamins (ACE) to reduce the genotoxic effect of CoCl 2 was proved.

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