![]() Likewise, nicotine can also activate the AKT pathway in the brain in a beneficial manner. In contrast, when the AKT pathway is activated in the brain after head injury or stroke, cannabinoids protect against cell death to the organism's benefit. The very cells that have accumulated sufficient genetic damage to normally initiate the apoptotic cascade are prevented from going down this suicidal path even though it would be best for the organism as a whole. However, the anti-apoptotic response that results from the stimulation of the nicotine receptors, under mutagenic conditions, creates a worst-case scenario. They both contain hot gasses and irritating particulate matter (tars). Both types of smoke contain a complex mixture of compounds, some of which are carcinogenic. The differential expression of receptors may account for the apparent difference in carcinogenic activity that results from smoking tobacco compared to cannabis. Cannabinoid receptors are also widely distributed, but have not been reported in respiratory epithelial cells. Nicotine receptors are widely distributed and are found in the epithelial cells lining respiratory passages. In contrast, nicotine activates some CYP1A1 activities, thus potentially increasing the carcinogenic effects of tobacco smoke. Thus, despite potentially higher levels of polycyclic aromatic hydrocarbons found in cannabis smoke compared to tobacco smoke (dependent on what part of the plant is smoked), the THC present in cannabis smoke should exert a protective effect against pro-carcinogens that require activation. demonstrates that THC treatment of murine hepatoma cells caused a dose dependent increase in CYP1A1 gene transcription, while at the same time directly inhibiting the enzymatic activity of the gene product. Benzo pyrene is converted to its carcinogenic metabolite diol epoxide, which binds to specific hyper-mutable nucleotide sequences in the K-ras oncogene and p53 tumor suppressor. Polycyclic aromatic hydrocarbons found in smoke are pro-carcinogens that are converted to carcinogens by the enzymatic activity of the cytochrome P4501A1 oxidase protein (CYP1A1 gene product). However, cannabis and tobacco have additional pharmacological activities, both receptor-dependent and independent, that result in different biological endpoints. Smoke from tobacco and cannabis contains many of the same carcinogens and tumor promoters. ![]()
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