Evaluation of cytotoxicity of different tobacco product preparations

Arimilli, Subhashini; Damratoski, Brad E.; Bombick, Betsy; Borgerding, Michael F.; Prasad, G.L.

doi:10.1016/j.yrtph.2012.09.004

Cited by 40 publications

(52 citation statements)

References 48 publications

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“…TPM was collected on glass fiber filters (Cambridge), and the amount of TPM obtained determined by weight increase of the filter. The collected particulate phase was dissolved in dimethylsulfoxide (DMSO) to a tar concentration of 20 mg/ml stock solution; DMSO was used as solvent control [12,13].…”

Section: Tobacco Product Preparations and Chemical Analysismentioning

confidence: 99%

“…Following previously established protocols [12], Phenol Red-free media were used for these preparations (DMEM without Phenol Red for 101A, 101B cells; Invitrogen Epi-Life media for HGECs). Mainstream smoke was passed through the respective media yielding a 20% stock solution (2 cigarettes per 10 ml media); parent media was used as solvent control [12,13]. For each condition, the dilution factors and NIC equivalents delivered are listed in Table S1.…”

Section: Tobacco Product Preparations and Chemical Analysismentioning

confidence: 99%

“…The low dose (14 ug/ml) represented the level of nicotine in the combustible TPP exposures, while the high dose (474 ug/ml) was used to reach exposure level nearing the cytotoxic response in the TPP exposures. The high NIC dose was chosen in this range because it was previously shown that NIC at close to millimolar doses had some cytotoxic effects on other cell types [12] and since we had determined such range yielded 20% cytotoxicity in oral cells [13]. NIC vs DMSO group comparisons were used mainly as controls for exposure and were not included for microarray expression profiling in the 101B cell line.…”

Section: Treatmentsmentioning

confidence: 99%

“…Cigarette smoke or its components cause DNA mutations and chromosomal damage, protein modifications, and expression changes of genes involved in cell death, inflammation, DNA repair and cell cycle regulation [4,[7][8][9][10][11]. In addition, the molecular response to cigarette smoke exposure is cell-and tissue-specific and varies with the type of exposed target organ and tobacco product [7,12,13].…”

Section: Introductionmentioning

confidence: 99%

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AKR1C1 as a Biomarker for Differentiating the Biological Effects of Combustible from Non-Combustible Tobacco Products

Woo¹,

Gao

Henderson³

et al. 2017

Preprint

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Smoking has been established as a major risk factor for developing oral squamous cell carcinoma (OSCC), but less attention has been paid to the effects of smokeless tobacco products. Our objective is to identify potential biomarkers to distinguish the biological effects of combustible tobacco products from those of non-combustible using oral cell lines. Normal human gingival epithelial cells (HGEC), non-metastatic (101A) and metastatic (101B) OSCC cell lines were exposed to different tobacco product preparations (TPPs) including cigarette smoke total particulate matter (TPM), whole-smoke conditioned media (WS-CM), smokeless tobacco extract in complete artificial saliva (STE), or nicotine (NIC) alone. We performed microarray-based gene expression profiling and found 3456 probe sets from 101A, 1432 probe sets from 101B, and 2717 probe sets from HGEC to be differentially expressed. Gene Set Enrichment Analysis (GSEA) revealed xenobiotic metabolism and steroid biosynthesis were the top two pathways that were upregulated by combustible but not by non-combustible TPPs. Notably, aldo-keto reductase genes, AKR1C1 and AKR1C2, were the core genes in the top enriched pathways and were statistically upregulated more than 8 fold by combustible TPPs. Our qRT-PCR results statistically support AKR1C1 as a potential biomarker for differentiating the biological effects of combustible from non-combustible tobacco products.

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Section: Tobacco Product Preparations and Chemical Analysismentioning

confidence: 99%

Section: Tobacco Product Preparations and Chemical Analysismentioning

confidence: 99%

Section: Treatmentsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

AKR1C1 as a Biomarker for Differentiating the Biological Effects of Combustible from Non-Combustible Tobacco Products

Woo¹,

Gao

Henderson³

et al. 2017

Preprint

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show abstract

“…Dentre os principais hábitos prejudiciais e capazes de induzir o câncer estão o etilismo e tabagismo (225,226) . O hábito do tabagismo, por exemplo, leva ao contato direto de substâncias nocivas com células epiteliais, as quais podem ter seu DNA danificado e não reparado, contribuindo para o processo de carcinogênese (227) .…”

Section: Discussionunclassified

Análise da expressão e mecanismos de ação das proteínas Akt, Hsp90, mTOR e ciclina D1 em cultura de células de carcinoma epidermoide humano e células displásicas após irradiação com laser em baixa intensidade

Sperandio¹

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Role of Oxidative Stress in the Suppression of Immune Responses in Peripheral Blood Mononuclear Cells Exposed to Combustible Tobacco Product Preparation

et al. 2017

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Cigarette smoking is a major risk factor for several human diseases. Chronic inflammation, resulting from increased oxidative stress, has been suggested as a mechanism that contributes to the increased susceptibility of smokers to cancer and microbial infections. We have previously shown that whole-smoke conditioned medium (WS-CM) and total particulate matter (TPM) prepared from Kentucky 3R4F reference cigarettes [collectively called as combustible tobacco product preparations (TPPs)] potently suppressed agonist-stimulated cytokine secretion and target cell killing in peripheral blood mononuclear cells (PBMCs). Here we have investigated the role of oxidative stress from TPPs, which alters inflammatory responses in vitro. Particularly, we investigated the mechanisms of WS-CM-induced suppression of select cytokine secretions in Toll-like receptor (TLR) agonist-stimulated cells and target cell killing by effector cells in PBMCs. Pretreatment with N-acetyl cysteine (NAC), a precursor of reduced glutathione and an established anti-oxidant, protected against DNA damage and cytotoxicity caused by exposure to WS-CM. Similarly, secretion of tumor necrosis factor (TNF), interleukin (IL)-6, and IL-8 in response to TLR-4 stimulation was restored by pretreatment with NAC. Target cell killing, a functional measure of cytolytic cells in PBMCs, is suppressed by WS-CM. Pretreatment with NAC restored the target cell killing in WS-CM treated PBMCs. This was accompanied by higher perforin levels in the effector cell populations. Collectively, these data suggest that reducing oxidative stress caused by cigarette smoke components restores select immune responses in this ex vivo model.

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Evaluation of cytotoxicity of different tobacco product preparations

Cited by 40 publications

References 48 publications

AKR1C1 as a Biomarker for Differentiating the Biological Effects of Combustible from Non-Combustible Tobacco Products

AKR1C1 as a Biomarker for Differentiating the Biological Effects of Combustible from Non-Combustible Tobacco Products

Análise da expressão e mecanismos de ação das proteínas Akt, Hsp90, mTOR e ciclina D1 em cultura de células de carcinoma epidermoide humano e células displásicas após irradiação com laser em baixa intensidade

Role of Oxidative Stress in the Suppression of Immune Responses in Peripheral Blood Mononuclear Cells Exposed to Combustible Tobacco Product Preparation

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