Browsing by Author "Truman P"

Now showing 1 - 7 of 7
  • Thumbnail Image
    Item
    Biologically Active Compounds Present in Tobacco Smoke: Potential Interactions Between Smoking and Mental Health
    (Frontiers Media SA, 26/04/2022) Hong SW; Teesdale-Spittle P; Page R; Ellenbroek B; Truman P
    Tobacco dependence remains one of the major preventable causes of premature morbidity and mortality worldwide. There are well over 8,000 compounds present in tobacco and tobacco smoke, but we do not know what effect, if any, many of them have on smokers. Major interest has been on nicotine, as well as on toxic and carcinogenic effects and several major and minor components of tobacco smoke responsible for the negative health effects of smoking have been elucidated. Smokers themselves report a variety of positive effects from smoking, including effects on depression, anxiety and mental acuity. Smoking has also been shown to have protective effects in Parkinson's Disease. Are the subjective reports of a positive effect of smoking due to nicotine, of some other components of tobacco smoke, or are they a manifestation of the relief from nicotine withdrawal symptoms that smoking provides? This mini-review summarises what is currently known about the components of tobacco smoke with potential to have positive effects on smokers.
  • Thumbnail Image
    Item
  • Thumbnail Image
    Item
    Hepatotoxicity of titanium dioxide nanoparticles.
    (John Wiley & Sons Ltd, 2024-05-13) Khan J; Kim ND; Bromhead C; Truman P; Kruger MC; Mallard BL
    The food additive E171 (titanium dioxide, TiO2), is widely used in foods, pharmaceuticals and cosmetics. It is a fine white powder, with at least one third of its particles sized in the nanoparticulate (˂100 nm range, TiO2 NPs). The use of E171 is controversial as its relevant risk assessment has never been satisfactorily accomplished. In vitro and in vivo studies have shown dose-dependent toxicity in various organs including the liver. TiO2 NPs have been shown to induce inflammation, cell death and structural and functional changes within the liver. The toxicity of TiO2 NPs in experimental models varies between organs and according to their physiochemical characteristics and parameters such as dosage and route of administration. Among these factors, ingestion is the most significant exposure route, and the liver is a key target organ. The aim of this review is to highlight the reported adverse effects of orally administered TiO2 NPs on the liver and to discuss the controversial state of its toxicity.
  • Thumbnail Image
    Item
    Monoamine oxidase (MAO) inhibitory effects of candidate MAO inhibitors found in cigarette smoke.
    (23/11/2021) Niraula P; Palmer B; Truman P; Page R
    There is strong evidence that tobacco smoke inhibits both MAO A and MAO B isoforms in the body. However, which components of cigarette smoke are responsible for MAO inhibition is not clear yet. Our group has identified six previously unidentified candidate MAO inhibitors from the tobacco smoke. The MAO inhibitory effects of these candidate inhibitors were compared with that of nicotine and TPM (Tobacco Particulate Matter). An SH-SY5Y cell line was exposed to different regimens of ethanol (control), nicotine, TPM and the cocktail of candidate inhibitors. A final concentration 0.2 μM nicotine was used and the concentration of each candidate inhibitor was relative to that originally found in TPM. We found that nicotine did not have any significant MAO inhibitory effect compared to the control. TPM inhibited overall MAO activity by 39%, while the MAO inhibition by cocktail of candidate inhibitors was 47%. The results suggest that the candidate inhibitors identified by our group are the major contributors to the total MAO inhibitory activity depicted by cigarette smoke and potentially unlocks the mystery behind the components responsible for MAO inhibition by cigarette smoke in smokers.
  • Thumbnail Image
    Item
    Potent inhibition of human monoamine oxidase A and B by phenolic compounds and polyunsaturated fatty acids in tobacco smoke
    (Elsevier B V, 2025-05-25) Hong SW; Heydari A; Watson PR; Teesdale-Spittle PH; Page R; Northcote PT; Keyzers RA; Vyssotski M; Truman P
    Smoking is a main cause of premature death and preventable disease in the world. Interestingly, animal studies indicate that inhibition of monoamine oxidase (MAO), key enzymes for the degradation of neurotransmitters, increased self-administration of nicotine. The purpose of this study was to identify and characterize the potential MAO inhibitors in tobacco smoke responsible for MAO inhibition in smokers. A bioassay-guided isolation from an extract of tobacco smoke showed that catechol, 4-methylcatechol, hydroquinone, α-linolenic acid, and linoleic acid all displayed potent human MAO inhibitory activity. Additionally, the tobacco catechols 4-ethylcatechol and 4-vinylcatechol were included to test their inhibitory potencies. Catechol, 4-methylcatechol, 4-ethylcatechol, and hydroquinone are potent and irreversible MAO inhibitors. Among the phenolic compounds tested, 4-methylcatechol and 4-ethylcatechol inhibited MAO A with IC50 values of 10.0 and 12.6 μM, respectively, reducing to 0.27 and 0.43 μM after 1 h preincubation. In addition, α-linolenic acid and linoleic acid competitively inhibited MAO A with Ki values of 10.50 and 6.95 μM, respectively. These results suggest that MAO inhibition by phenolics and polyunsaturated fatty acids in tobacco smoke may be important contributors to the MAO inhibition experienced by smokers and to the enhancement of nicotine dependence this MAO inhibition is believed to cause.
  • Thumbnail Image
    Item
    Proteins isolated with TRIzol are compatible with two-dimensional electrophoresis and mass spectrometry analyses
    (Elsevier Masson, 2012) Young C; Truman P
    TRIzol is used for RNA isolation but also permits protein recovery. We investigated whether proteins prepared with TRIzol were suitable for two-dimensional gel electrophoresis (2-DE) and matrix-assisted laser desorption/ionization mass spectrometry. Proteins from TRIzol-treated SH-SY5Y cells produced 2-DE spot patterns similar to those from an equivalent untreated sample. Subsequent identification of TRIzol-treated proteins using peptide mass fingerprinting was successful. TRIzol exposure altered neither the mass of myoglobin extracted from sodium dodecyl sulfate (SDS) gels nor the masses of myoglobin peptides produced by in-gel trypsin digestion. These findings suggest that proteins isolated with TRIzol remain amenable to proteomic analyses.
  • Thumbnail Image
    Item
    Smoking, coffee intake, and Parkinson's disease: Potential protective mechanisms and components.
    (Elsevier B.V., 2024-12-20) Hong SW; Page R; Truman P
    Parkinson's disease (PD) is a common progressive neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Environmental and lifestyle factors, such as smoking and coffee drinking, have been associated with a decreased risk for PD. However, the biological mechanisms underlying protective effects on PD are still not fully understood. It has been suggested that non-nicotine components in cigarette smoke and non-caffeine components in coffee may contribute to this protective effect. The aim of this review was to explore candidate molecules and mechanisms behind the effects of smoking and coffee drinking on PD by integrating findings from previous studies. By cross-referencing an index of tobacco constituents and a list of coffee constituents with existing literature on natural compounds and their structural analogs that show inhibitory activities against monoamine oxidase B, catechol O-methyltransferase, and α-synuclein fibrillation, we have identified tobacco and coffee components that inhibit these targets. Furthermore, tobacco and coffee components potentially play roles in suppressing neuroinflammation, activating the Nrf2 pathway as natural activators, and altering the gut microbiome. This review suggests that the phenolic compounds from tobacco and coffee investigated may contribute to the low incidence of PD in smokers and coffee drinkers, showing moderate to strong potential as therapeutic interventions. The current review suggests that multifunctional molecules found in coffee and cigarette smoke may have potential neuroprotective effects, but none of the data indicates that multifunctionality is required for these effects. This review will deepen our understanding of how smoking and coffee drinking are linked to a reduced risk of PD and will also be important in elucidating the mechanisms underlying the protective effects of smoking and coffee drinking on PD.