Genotoxicity of yellow shammah (smokeless tobacco) in murine bone marrow cells in vivo.

Shammah is a traditional form of smokeless tobacco (ST) that is manufactured and used locally by people of Middle East with highest usage in Saudi Arabia, Yemen and Sudan. In Saudi Arabia, shammah comes in three variants: white, brown and yellow. In the present study, we investigated the genotoxicity of yellow shammah (YS) on bone marrow (BM) cells in vivo using mice. Bone marrow (BM) chromosomal aberration (CA) and micronucleus (MN) assay were performed and hepatic markers of oxidative stress were determined. Swiss albino mice were divided into five groups (n = 6) including negative control (NC) and positive control (PC) groups. The three treated groups included YS-100, 200 and 300 mg/kg, doses freshly prepared in 0.5% carboxymethyl cellulose (CMC) and administered orally once a day for 2 weeks. PC animals were administered cyclophosphamide (CP) at a dose of 40 mg/kg body weight, 24 h before termination. Two weeks continuous treatment of YS induced a dose dependent and significant increase in aberrant metaphases (AM), CA per cell and depression in mitotic activity. In micronucleus assay, YS treatment increased the percentage of micronucleated polychromatic erythrocytes (MNPCE) frequency and showed statistically significant reduction in polychromatic erythrocyte/normochromatic erythrocyte ratio at all doses, as compared to NC. YS also markedly inhibited the activities of superoxide dismutase, reduced glutathione and increased malondialdehyde content. CP was used as clastogen (positive control) and yielded the expected positive results. Therefore, it may be concluded that YS has genotoxic and cytotoxic effects for BM cells of mice in vivo.

In vivo assessment of genotoxic potential of brown shammah (smokeless tobacco) in bone marrow cells of mice.

This study was aimed to assess the genotoxicity of brown shammah (BS), a local form of smokeless tobacco, popular in Middle East countries including Yemen, Saudi Arabia and Sudan. The genotoxicity was explored using in vivo chromosomal aberration (CA), micronucleus (MN) and sperm abnormality (SA) assays. In addition, oxidative stress was also determined using various hepatic markers. Swiss albino mice were selected for the study, which were divided in to 5 groups of six animals each. They include, negative control (NC, received only vehicle) as well as positive control group (PC, received vehicle for 2 weeks followed by administration of cyclophosphamide, CP). Depending upon their dose, three BS treated animal groups were BS-100, 300 and 900 mg/kg. Doses of BS were obtained by suspending BS in 0.5% CMC (carboxy methyl cellulose) and orally administered once a day for 2 weeks. Significant augmentation of the average percentage of aberrant metaphase (AM), CA per cells and suppressed mitotic activity was observed on post administration of BS. In addition, BS increased the occurrence of MNPCEs (micronucleated polychromatic erythrocytes) formation, induced cytotoxicity and increased percentage of abnormal sperms as compared to NC. Moreover, BS also induced oxidative stress as the activities of hepatic superoxide dismutase (SOD) and glutathione (GSH) were reduced and malondialdehyde (MDA) content were increased by BS. Cyclophosphamide was utilized as clastogen, showed anticipated positive results and confirmed the sensitivity of test system. Therefore, it may be deduced from the study that the BS possesses genotoxic effects on mice bone marrow and germ cells in vivo.