Adverse effects of Sudanese<i>toombak</i>vs. Swedish snuff on human oral cells

Costea, Daniela Elena; Lukandu, Ochiba M.; Bui, Linh; Ibrahim, Muna Jaffar M.; Lygre, Raymond; Neppelberg, Evelyn; Ibrahim, Mohamed Yousif; Vintermyr, Olav Karsten; Johannessen, Anne Christine

doi:10.1111/j.1600-0714.2009.00825.x

Cited by 26 publications

(19 citation statements)

References 34 publications

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“…Their have been several reports regarding STE-induced cytotoxicity [12]–[14], but the exact molecular mechanism is still uncertain. Exposure to STE is known to cause cell death and apoptosis in several cultured cell lines including oral keratinocytes [12], [15], and macrophages [16].…”

Section: Introductionmentioning

confidence: 99%

Smokeless Tobacco Extract (STE)-Induced Toxicity in Mammalian Cells is Mediated by the Disruption of Cellular Microtubule Network: A Key Mechanism of Cytotoxicity

et al. 2013

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Smokeless tobacco usage is a growing public health problem worldwide. The molecular mechanism(s) underlying smokeless tobacco associated tissue damage remain largely unidentified. In the present study we have tried to explore the effects of aqueous extract of smokeless tobacco (STE) on tubulin-microtubule, the major cytoskeleton protein that maintains cells morphology and participates in cell division. Exposure to STE resulted in dose-dependent cytotoxicity in a variety of mammalian transformed cell lines such as human lung epithelial cells A549, human liver epithelial cells HepG2, and mouse squamous epithelial cells HCC7, as well as non-tumorogenic human peripheral blood mononuclear cells PBMC. Cellular morphology of STE-treated cells was altered and the associated disruption of microtubule network indicates that STE targets tubulin-microtubule system in both cell lines. Furthermore it was also observed that STE-treatment resulted in the selective degradation of cellular tubulin, whereas actin remains unaltered. In vitro, polymerization of purified tubulin was inhibited by STE with the IC50 value∼150 µg/ml and this is associated with the loss of reactive cysteine residues of tubulin. Application of thiol-based antioxidant N-acetyl cysteine (NAC) significantly abrogates STE-mediated microtubule damage and associated cytotoxicity in both A549 and HepG2 cells. These results suggest that microtubule damage is one of the key mechanisms of STE-induced cytotoxity in mammalian cells.

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Section: Introductionmentioning

confidence: 99%

Smokeless Tobacco Extract (STE)-Induced Toxicity in Mammalian Cells is Mediated by the Disruption of Cellular Microtubule Network: A Key Mechanism of Cytotoxicity

et al. 2013

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“…It contains at least 100-fold higher concentrations of the carcinogenic factor tobacco specific N-nitrosamines compared with American and Swedish commercial snuff brands [53]. A recent study showed that toombak induces DNA damage and cell death in normal human oral cells more than the Swedish snuff [54]. …”

Section: Discussionmentioning

confidence: 99%

Oral mucosal lesions in skin diseased patients attending a dermatologic clinic: a cross-sectional study in Sudan

et al. 2011

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BackgroundSo far there have been no studies focusing on the prevalence of a wide spectrum of oral mucosal lesions (OML) in patients with dermatologic diseases. This is noteworthy as skin lesions are strongly associated with oral lesions and could easily be neglected by dentists. This study aimed to estimate the frequency and socio-behavioural correlates of OML in skin diseased patients attending outpatient's facility of Khartoum Teaching Hospital - Dermatology Clinic, Sudan.MethodsA cross-sectional hospital-based study was conducted in Khartoum from October 2008 to January 2009. A total of 588 patients (mean age 37.2 ± 16 years, 50.3% females) completed an oral examination and a personal interview of which 544 patients (mean age 37.1 ± 15.9 years, 50% females) with confirmed skin disease diagnosis were included for further analyses. OML were recorded using the World Health Organization criteria (WHO). Biopsy and smear were used as adjuvant techniques for confirmation. Data were analysed using the Statistical Package for Social Science (Version 15.0.1). Cross tabulation and Chi-square with Fisher's exact test were used.ResultsA total of 438 OML were registered in 315 (57.9%, males: 54.6% versus females: 45.6%, p < 0.05) skin diseased patients. Thus, a certain number of patients had more than one type of OML. Tongue lesions were the most frequently diagnosed OML (23.3%), followed in descending order by white lesions (19.1%), red and blue lesions (11%) and vesiculobullous diseases (6%). OML in various skin diseases were; vesiculobullous reaction pattern (72.2%), lichenoid reaction pattern (60.5%), infectious lesions (56.5%), psoriasiform reaction pattern (56.7%), and spongiotic reaction pattern (46.8%). Presence of OML in skin diseased patients was most frequent in older age groups (62.4% older versus 52.7% younger, p < 0.05), in males (63.2% males versus 52.6% females, p < 0.05), patients with a systemic disease (65.2% with systemic versus 51.9% without systemic disease, p < 0.05) and among current users of smokeless tobacco (toombak) (77% current use versus 54.8% no use, p < 0.00).ConclusionsOML were frequently diagnosed in skin diseased patients and varied systematically with age, gender, systemic condition and use of toombak. The high prevalence of OML emphasizes the importance of routine examination of oral mucosa in a dermatology clinic.

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“…There have been reports of cytotoxicity caused by smokeless tobacco products such as gutkha (Avti et al, 2010), khaini (Das et al, 2013), Sudanese toombak (Costea et al, 2010), American moist snuff (Misra et al, 2014), Swedish moist snuff (Coggins et al, 2012, Costea et al, 2010, Kentucky reference moist smokeless tobacco product (Lombard et al, 2010) and commercial chewing tobacco (Coppe et al, 2008). The present study is the first assessment of cytotoxicity induced by tobacco constituents of pituri as a means of investigating its potential carcinogenicity.…”

Section: Introductionmentioning

confidence: 96%

“…Toombak is the only indigenous smokeless tobacco that has been studied for its cytotoxicity and the results indicated its higher toxic potential compared to commercially available Swedish snuff (Costea et al, 2010). There is very little information available on the extent of toxicity caused by indigenous or local smokeless tobacco products similar to pituri.…”

Section: Toxicity Of Smokeless Tobacco Productsmentioning

confidence: 99%

“…There are numerous reports on in vitro cytotoxic effects of commercially available smokeless tobacco products such as Swedish snus (Coggins et al, 2012, Costea et al, 2010, American moist snuff (Misra et al, 2014), commercial chewing tobacco (Coppe et al, 2008) and Kentucky reference smokeless tobacco product (Lombard et al, 2010). There have been reports of cytotoxicity caused by Indian manufactured smokeless tobacco such as gutka (Avti et al, 2010) and khaini (Das et al, 2013).…”

Section: Toxicity Of Smokeless Tobacco Productsmentioning

confidence: 99%

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Investigations into the pituri plant: nicotine content, nicotine conversion to nornicotine, nicotine release and cytotoxicity of Australian native Nicotiana spp.

Moghbel¹

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The Aboriginal population of Central Australia use endemic Nicotiana spp. to make a smokeless tobacco product known as pituri that they chew/suck for nicotine absorption. This thesis describes the relative abundance of nicotine alkaloids amongst Australian Nicotiana spp., with special focus on the molecular characteristics of nicotine to nornicotine conversion.The most popular chewed species, N. gossei, is investigated for nicotine release and cytotoxicity in comparison to similar products to gain insight into potential hazards to pituri users.To analyse the alkaloids of Nicotiana leaves, a HPLC-UV method was developed to separate and quantify six closely related alkaloids (nicotine, nornicotine, anatabine, anabasine, myosmine, cotinine). A C18 column with a mobile phase of ammonium formate buffer (pH 10.5) separated the six alkaloids within 13 min with detection at 260 nm. Linearity, precision and reproducibility were satisfactory. The limit of quantification was 2.8 and 4.8 µg/mL for nornicotine and nicotine, respectively, and below 2 µg/mL for other alkaloids. This method quantifies more alkaloids and in less time than previously reported methods.Tobacco alkaloids are responsible in formation of carcinogenic tobacco specific nitrosamines such as N'-nitrosonornicotine (NNN) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). To quantify NNN and NNK, a fast LC-MS/MS method was developed using a HILIC column with a triple quadrupole tandem mass spectrometry. The linearity, accuracy, recovery and repeatability for this method were satisfactory, with quantification limit of 2.6 and 4.3 ng/mL for NNN and NNK, respectively. Nornicotine results from demethylation of nicotine, and is associated with negative effects on health. A group of cytochrome P450 genes that are mainly expressed during senescence or drying is involved in this conversion. The conversion loci were amplified in all studied 24 taxa, and sequenced in 6 selected species that contrast in conversion phenotype. Transcript accumulation of the responsible loci in fresh versus dried leaves of low or nonconverter N. gossei, N. excelsior and N. benthamiana maintained a steady level or a slight increase, but increased by 3 fold in cured leaves of the high converter N. goodspeedii, N. velutina and N. cavicola. This indicates the presence of functional loci that are triggered by curing only in high ii converter species and poses a potential risk for chewers of these species due to their greater potential for nornicotine production.The release of nicotine from the leaves of N. gossei was compared to that from a Swedish snus, the CORESTA reference smokeless tobacco (CRP2), and Nicabate chewing gum. A model buccal cavity system was developed and three different chewing conditions, performed manually were tested over 120 minutes: no chewing action, initial chewing and chewing at 15-minute intervals. To simulate the effect of alkaline wood ash, the effect of alkaline pH on the release of nicotine from N. gossei dry leaves was also evaluated. Samples ...

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Adverse effects of Sudanesetoombakvs. Swedish snuff on human oral cells

Cited by 26 publications

References 34 publications

Smokeless Tobacco Extract (STE)-Induced Toxicity in Mammalian Cells is Mediated by the Disruption of Cellular Microtubule Network: A Key Mechanism of Cytotoxicity

Smokeless Tobacco Extract (STE)-Induced Toxicity in Mammalian Cells is Mediated by the Disruption of Cellular Microtubule Network: A Key Mechanism of Cytotoxicity

Oral mucosal lesions in skin diseased patients attending a dermatologic clinic: a cross-sectional study in Sudan

Investigations into the pituri plant: nicotine content, nicotine conversion to nornicotine, nicotine release and cytotoxicity of Australian native Nicotiana spp.

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