Browsing by Subject "Nicotine"

Now showing 1 - 5 of 5
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    Editorial: Molecular mechanisms in psychiatry 2023: addictive disorders.
    (Frontiers, 2025-02-17) Fernández López, Lucía; Almela Rojo, Pilar; Falcón Romero, María; Navarro Zaragoza, Javier; Farmacología
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    Genetic susceptibility to nicotine and/or alcohol addiction: a systematic review
    (Taylor and Francis Group, 2019-05-23) Pérez Cárceles, María D.; Calle, Irene de la; Arjona, Fuensanta; Roca, Miriam; Cejudo, Pablo; Luna, Aurelio; Osuna, Eduardo; Legaz Pérez, Isabel; Ciencias Sociosanitarias
    Recent studies have confirmed the wide consumption of tobacco and alcohol in our society and the strong addiction generated by these substances, which is responsible for high public health expenditure. Understanding the biological mechanisms of nicotine and/or alcohol dependence should have huge public health repercussions in the future. The aim of this review was to analyze the main human genes and polymorphisms related to nicotine and/or alcohol addiction, to help understand the biological mechanisms involved and which may be useful for developing new treatments in the future.
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    Harmine shows therapeutic activity on nicotine-induced liver failure in mice
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2019) Salahshoor, Mohammad Reza; Gholami mahmoudian, Zahra; Roshankhah, Shiva; Farokhi, Mehdi; Jalili, Cyrus
    This experiment evaluated the effects of harmine against nicotine-induced damage to the liver of mice. Nicotine is a major toxic component of cigarette smoke and a major risk factor for functional disorders in the liver, because it induces oxidative stress. Harmine is a harmal-derived alkaloid with therapeutic and antioxidant properties. In this study, 80 male mice were randomly assigned to 10 groups: the normal control and nicotine control groups (2.5 mg/kg); the harmine groups (5, 10, 15, and 20 mg/kg), and the nicotine + harmine groups (5, 10, 15 and 20 mg/kg mg/kg). Treatments were administered intraperitoneally daily for 28 days. Nitric oxide (NO) level, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) concentrations were determined. In addition, thiobarbituric acid reactive species, antioxidant capacity, and the diameters of the hepatocytes and central hepatic vein (CHV) were investigated. Nicotine administration significantly improved liver MDA and NO levels, CHV and hepatocyte diameters, and liver enzymes, and it decreased tissue FRAP levels compared to the normal control group (p<0.05). In the harmine and harmine + nicotine groups, in all dosages, all measured factors decreased significantly, while the FRAP tissue level increased compared with the nicotine control group (p<0.05). It seems that liver injury was improved by harmine administration in mice because of nicotine.
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    Influence of nicotine and caffeine on rat embryonic development
    (Murcia : F. Hernández, 1988) Nash, J.E.; Persaud, T.V.N.
    The influence on embryonic development of nicotine and caffeine at dose levels approximating human consumption was investigated in Sprague- Dawley rats. One group of animals received nicotine administered subcutaneously by an Alzet mini-osmotic pump from gestational day 6 through 12 (25 mg over 7 days; rate 149 pg/hr). Control animals received physiological saline in a similar manner. A second group received a single intravenous injection of caffeine (25 mg/ kg) on gestational day 6. Control animals were treated with physiological saline. A further group received both nicotine and caffeine on gestational day 6 as described for the two previous groups. There were no significant differences among any of the groups with respect to maternal weight gain, litter size, embryolethality, fetal weight, or crown-rump length. The offspring of nicotine treated animals showed a significantly higher incidence of hydrocephaly when compared to the controls, but in the combined treatment group no malformed fetuses were observed. Light microscopic examination of maternal liver, kidney and placentas revealed changes in the hepatic sinusoids, glomeruli and intervillous spaces after nicotine and combined treatment. In addition, the decidua basalis was poorly developed compared to the controls. Chorionic villi and fetal kidney appeared normal in al1 groups. A coteratogenic effect is not evident from these findings.
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    The effects of cigarette smoking and nicotine on the therapeutic potential of mesenchymal stem cells
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Harrell, Carl Randall; Djonov, Valentin; Volarevic, Vladislav
    Due to their immunoregulatory properties and capacity for multi-lineage differentiation, mesenchymal stem cells (MSCs) have been used as new therapeutic agents in regenerative medicine. Numerous lifestyle habits and behavioral risk factors may modulate metabolic and cell growth signaling pathways in MSCs, affecting their phenotype and function. Accordingly, identification of these factors and minimization of their influence on viability and function of transplanted MSCs may greatly contribute to their better therapeutic efficacy. A large number of experimental and clinical studies have demonstrated the detrimental effects of cigarette smoke and nicotine on proliferation, homing, chondrogenic and osteogenic differentiation of MSCs. Cigarette smoke down-regulates expression of chemokine receptors and modulates activity of antioxidative enzymes in MSCs, while nicotine impairs synthesis of transcriptional factors that regulate the cell cycle, metabolism, migration, chondrogenesis and osteogenesis. In this review article, we summarize current knowledge about molecular mechanisms that are responsible for cigarette smoke and nicotine-dependent modulation of MSCs' therapeutic potential.