Nicotine and caffeine-mediated modulation in the expression of toxicant responsive genes and vesicular monoamine transporter-2 in 1-methyl 4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson's disease phenotype in mouse

Singh, Seema; Singh, Kavita; Patel, Suman; Patel, Devendra Kumar; Singh, Chetna; Nath, Chandishwar; Singh, Mahendra Pratap

doi:10.1016/j.brainres.2008.02.023

Cited by 45 publications

(29 citation statements)

References 56 publications

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“…Since caffeine metabolism to paraxanthine is a specific probe reaction for CYP1A2 [13], it can be concluded that CYP1A2 activity is not affected by 8 days of nicotine dosing. Although previous studies in experimental animals have provided evidence for the role of nicotine in the induction of CYP1A1 and CYP1A2 enzymes [4][5][6][7][8][9][10], our study disproves the hypothesis that nicotine induces CYP1A2 activity in humans in vivo. The discrepancy between human and animal data may be explained by tissue and species specific expression patterns.The human caffeine phenotyping probes the hepatic CYP1A2 activity, whereas the animal studies are mainly on extrahepatic CYP1A1 induction or based on methods not capable of differentiating between CYP1A1 and CYP1A2 enzymes.…”

contrasting

confidence: 73%

Effect of nicotine on cytochrome P450 1A2 activity

Hukkanen

Jacob

Peng

et al. 2011

Brit J Clinical Pharma

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Cigarette smoking accelerates the metabolism of certain drugs, particularly those primarily metabolized by cytochrome P450 1A2 (CYP1A2) and, to a lesser extent, CYP2E1 and some UDP-glucuronosyltransferases [1,2]. The induction of CYP1A2 is mediated by binding of polycyclic aromatic hydrocarbons of the tobacco smoke to the aryl hydrocarbon receptor (AHR) with consequent transcriptional activation of the CYP1A2 gene. Furthermore, CYP1A1 and CYP1B1 enzymes are induced by tobacco smoking via AHR in various human tissues such as lung and placenta [3]. As CYP1A1 and CYP1B1 are mostly expressed in extrahepatic tissues, their induction by smoking is not known to affect the pharmacokinetics of any medication. There is evidence of the role of nicotine in the induction of CYP1A1 and CYP1A2 enzymes in vitro in rat lung [4], and in vivo in rat lung, kidney and liver [5][6][7], liver and placenta of pregnant rats [8] and in brains of mice and rats [9,10], probably through mechanisms not involving AHR. Some evidence exists for the induction of CYP1A1 by nicotine in human pulmonary explant culture [11].We recently published a study on the effects of 10 day dosing of nicotine on human CYP2A6 and CYP2E1 activities [12]. An additional aim of that study was to determine the effects of high dose nicotine on the pharmacokinetics of oral caffeine and to test the hypothesis that nicotine induces CYP1A2-mediated metabolism of caffeine to paraxanthine, a well-established probe reaction of CYP1A2 activity [13]. No previous study has studied the effects of nicotine on CYP1A2 activity in humans in vivo.The details of the experimental protocol and the subject characteristics are described in a prior report [12]. Briefly, 12 healthy smokers were given two 21 mg transdermal patches delivering a total of 42 mg nicotine day -1 or placebo patches, each for 10 days in a randomized and crossover design. Subjects were not allowed to smoke or to use any tobacco products during hospitalization. At noon on the eighth hospital day, 200 mg of oral caffeine was given. Blood samples were collected for measurement of caffeine and metabolites at 0, 30 and 60 min, and then 2, 3, 4, 6, 8, 12, 20, 32, 44 and 52 h after ingestion of caffeine. In addition, deuterium-labelled nicotine-D2 and cotinine-D4 phenotyping for CYP2A6, bupropion phenotyping for CYP2B6 and chlorzoxazone phenotyping for CYP2E1 were performed on the seventh and eighth hospital days as previously described [12].Concentrations of caffeine, paraxanthine, theobromine and theophylline in plasma were determined using liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS). Stable isotope-labelled analogues of paraxanthine and caffeine were used as internal standards. Following protein precipitation, samples (0.2 ml) were treated with phosphate buffer and extracted with a mixture of methylene chloride, ethyl acetate and isopropyl alcohol. The extracts were evaporated, reconstituted in the LC mobile phase, and injected into the LC-MS/MS system. The mass spectrometer was operated using ...

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confidence: 73%

Effect of nicotine on cytochrome P450 1A2 activity

Hukkanen

Jacob

Peng

et al. 2011

Brit J Clinical Pharma

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“…The results in this study demonstrate that the tested pharmaceuticals resulted in a significant GST induction in goldfish, and they all showed full bell shaped concentration-response curves. The induction of GST activity was observed in crustacean and mouse when exposed to methotrexate and therapeutic agents (Nunes et al 2006;Singh et al 2008). Furthermore, GST activity in liver tissue of Oreochromis niloticus was induced by feeding with sulfamethoxazole ).…”

Section: Resultsmentioning

confidence: 98%

Single and combined effects of selected pharmaceuticals at sublethal concentrations on multiple biomarkers in Carassius auratus

Yang

et al. 2011

Ecotoxicology

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In this study, the sublethal effects of caffeine, sulfamethoxazole and their mixture on goldfish (Carassius auratus) were investigated, the biomarkers including acetylcholinesterase (AChE) in brain, 7-ethoxyresorufin O-deethylase (EROD), glutathione S-transferase (GST) and superoxide dismutase (SOD) in liver and vitellogenin (VTG) in serum were determined after 1, 2, 4, and 7 days of exposure. AChE activity was significantly inhibited by caffeine (≥0.4 mg/l), sulfamethoxazole (≥0.4 mg/l) and their mixtures (≥0.048 mg/l) during all exposure periods, and obvious concentration-response and time-response relationships were obtained. EROD, GST and SOD activities were significantly increased by individual compounds and mixtures in most cases. GST induction exhibited bell-shaped concentration-response curves. Serum VTG was significantly induced by 2 mg/l of caffeine, 10 mg/l of sulfamethoxazole and the mixtures at concentrations ≥1.2 mg/l. In general, the two pharmaceuticals induced similar biological responses. The joint effect of caffeine/sulfamethoxazole was additive with regard to AChE and GST activity variation and was antagonistic with regard to EROD and SOD induction. The results indicated that multiple biomarker response method might be a useful tool for describing an integrated toxicological effect of chemicals. VTG induction suggested that caffeine and sulfamethoxazole may cause a slightly feminization effect.

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“…An inverse relationship between PD and caffeine consumption is reported in epidemiological and animal based studies [8,[17][18][19][20]. The neuroprotective effects of caffeine are reported to be mediated by its antagonistic action on adenosine A 2A receptor, leading to enhanced dopamine release into the striatum [13].…”

Section: Introductionmentioning

confidence: 96%

“…The neuroprotective effects of caffeine are reported to be mediated by its antagonistic action on adenosine A 2A receptor, leading to enhanced dopamine release into the striatum [13]. Additionally, its phosphodiesterase inhibitory activity leads to pronounced availability of cyclic adenosine monophosphate, which augments the protein kinase activity, thereby enhancing the expression of growth factors, modulation of toxicant responsive genes and anti-apoptotic property [8,[19][20][21][22][23][24][25].…”

Section: Introductionmentioning

confidence: 99%

Role of Secondary Mediators in Caffeine-Mediated Neuroprotection in Maneb- and Paraquat-Induced Parkinson’s Disease Phenotype in the Mouse

et al. 2011

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Maneb and paraquat are known to induce Parkinson's disease (PD) phenotype, however, caffeine offers neuroprotection. Nitric oxide (NO) acts an important mediator in PD phenotype and tyrosine kinase (TK), nuclear factor kappa B (NF-kB), p38 mitogen activated protein kinase (p38 MAPK) are known to regulate its production. The present study aimed to elucidate the role of caffeine in the regulation of NO production and microglial activation and their subsequent contribution in dopaminergic neuroprotection. The animals were treated with caffeine and/or maneb and paraquat along with controls. In a few sets of experiments, the animals were also treated with aminoguanidine, an inhibitor of inducible NO synthase, pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-kB, genistein, an inhibitor of TK or SB202190, an inhibitor of p38 MAPK. Tyrosine hydroxylase (TH)-immunoreactivity and anti-integrin αM (OX-42) staining were performed to assess the number of dopaminergic neurons and activation of microglia, respectively. NO was measured in terms of nitrite, however, the expressions of p38 MAPK, interleukin (IL)-1β, NF-kB and TK were checked by western blot analyses. Maneb and paraquat induced the number of degenerating dopaminergic neurons, microglial cells, nitrite content, expressions of IL-1β, p38 MAPK, NF-kB and TK and caffeine co-treatment reduced the level of such alterations. Reductions were more pronounced in the animals co-treated with aminoguanidine, PDTC, genistein or SB202190. The results obtained thus demonstrate that caffeine down-regulates NO production, neuroinflammation and microglial activation, which possibly contribute to neuroprotection.

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Nicotine and caffeine-mediated modulation in the expression of toxicant responsive genes and vesicular monoamine transporter-2 in 1-methyl 4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson's disease phenotype in mouse

Cited by 45 publications

References 56 publications

Effect of nicotine on cytochrome P450 1A2 activity

Effect of nicotine on cytochrome P450 1A2 activity

Single and combined effects of selected pharmaceuticals at sublethal concentrations on multiple biomarkers in Carassius auratus

Role of Secondary Mediators in Caffeine-Mediated Neuroprotection in Maneb- and Paraquat-Induced Parkinson’s Disease Phenotype in the Mouse

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