Nicotine Oral Administration Attenuates DSS-Induced Colitis Through Upregulation of Indole in the Distal Colon and Rectum in Mice

Nicotine affects the gastrointestinal environment and modulates ulcerative colitis (UC). However, the associations among nicotine, gut metabolites, and UC are still largely unknown. We investigated whether orally administered nicotine affected gut metabolites and dextran sodium sulfate (DSS)-induced colitis. C57BL/6 male mice were orally administered nicotine solution in drinking water prior to inducing DSS-induced colitis. Short-chain fatty acids (SCFAs) and indole in gut contents and fecal samples were measured by GC-MS and hydroxylamine-based indole assays, respectively. Oral administration of nicotine increased indole concentration in feces, but, in contrast, SCFA values did not differ with nicotine administration. Indole levels were increased in the distal colon and rectum but not in the cecum and proximal colon. DSS-induced colitis was less severe clinically and histological changes were minimal in the rectum of orally nicotine-administered mice compared to mice drinking only water. 16S rRNA microbiome on the feces revealed an increasing in Clostridium and Porphyromonas in nicotine-administered mice. In conclusion, nicotine administration was associated with increased indole levels in the distal colon and rectum and attenuated DSS-induced colitis. Oral administration of nicotine may play a potential role in indole upregulation and prevention of UC.

Nicotine exacerbates reproductive biomarkers via generation of free radicals in female Wistar rats: Protective role of Quercetin

Background: Nicotine has been widely reported to generate free radicals in several organs of the body. Therefore, this study investigated the ameliorative potentials of Quercetin on selected reproductive biomarkers in female Wistar rats.Methods: Forty female rats were randomly divided into five groups (n=8) which were treated as follows: Group I (CN) received normal saline (1 ml/kg bwt); Group II (LN) received nicotine (0.5 mg/kg bwt) only; Group III (HN) received nicotine (1.0 mg/kg bwt) only; however, Groups IV (LNA) and V (HNA) received 0.5 and 1.0 mg/kg of nicotine with 20 mg/kg of quercetin respectively. All administration were done orally and lasted 28 days. Results: Nicotine significant reduction in the bioavailability of estrogen and progesterone in the treated rats when compared to control. Furthermore, relative to the control group, nicotine administration resulted in significant elevation in MDAand consequently caused significant reduction in the antioxidant enzymes (SOD and CAT) activities. However, quercetin treatment ameliorated these alterations. Conclusion: Quercetin dampens the reproductive distruptive effects exerted by nicotine through anti-oxidative mechanism in female Wistar rats.

The effects of moxidectin nicotine-conditioned cue on nicotine-seeking behavior in mice

Current pharmacotherapies for nicotine abuse are few and relatively inefficient demonstrating the need for the development of new, effective remedies. Moxidectin is used as an anti-parasitic agent in both animals and humans, it also activates GABA receptors. The objective of the present investigation was to study the effect of moxidectin on nicotine-induced conditioned place preference (CPP) in male Swiss mice. Intraperitoneal (i.p.) route was used for nicotine (0.5mg/kg) administration for a 3-day conditioning program. The influences of moxidectin on the reinforcing characteristics of nicotine were tested in mice given i.p. treatment of moxidectin (5 and 10mg/kg) 30 minutes prior to per nicotine administration. CPP was extinguished by repeated testing, through which conditioned mice were daily given two doses of moxidectin (5 and 10mg/kg, i.p.). Subsequently, the potency of moxidectin in blocking the reinstatement of CPP provoked by priming given low-dose nicotine (0.1mg/kg, i.p.) was also evaluated. Moxidectin treatment illustrated a reserve of acquisition of nicotine-induced CPP. It was reduced priming nicotine-induced reinstatement and accelerated the extinction of CPP. Relatively nicotine enhanced the locomotor, motor activity but was not statistically significant. In conclusion, the outcomes demonstrate the potential for the development of moxidectin as a new pharmacotherapy for the treatment of nicotine addiction.

A Neurochemical and Electrophysiological Study on the Combined Effects of Caffeine and Nicotine in the Cortex of Rats

Objective: Caffeine and nicotine are the most consumed psychostimulants worldwide. Although the effects of each drug alone on the central nervous system (CNS) were studied extensively, the literature on the neurochemical and electrophysiological effects of their combined treatments is scarce. The present study investigates the cortical electrophysiological and neurochemical alterations induced by acute administration of caffeine and nicotine in rats. Methods: Rats received caffeine and nicotine with 1h interval between the two treatments. Results: Caffeine and nicotine administration resulted in a significant decrease in the concentrations of cortical amino acid neurotransmitters namely glutamate, aspartate, glycine and taurine while γ-aminobutyric acid (GABA) was significantly increased. An increased cortical lipid peroxidation and decreased reduced glutathione and nitric oxide levels and acetylcholinesterase and Na+, K+-ATPase activities were also observed. The electroencephalogram (EEG) showed an increase in delta frequency power band while theta, beta-1 and beta-2 were decreased after caffeine and nicotine treatment. These findings suggest that caffeine and nicotine adversely exacerbate their stimulant effects. This was manifested by the EEG changes and mediated by increasing cholinergic transmission, disturbing the balance between the excitatory and inhibitory amino acids leading to oxidative stress.

Influence of nicotine upon human brain metabolism, an in vivo noninvasive Near Infrared Spectroscopy (NIRS) study

Nicotine, a natural alkaloid derived from tobacco, is involved in various outcomes ranging from addiction to toxicity and/or neuro-protective actions. Nevertheless, the literature on the effects of nicotine administration upon the activity of brain regions is mixed; either increased, decreased, or no overall effect was reported when being evaluated by various methodologies such as positron emission tomography (PET), functional Magnetic Resonance Imaging (fMRI). In this work, Near Infrared Spectroscopy (NIRS) is applied as it allows monitoring oxygen saturation in the living tissue as well as changes in oxygenation of hemoglobin and when applied on brain studies, it gives indications of cerebral haemo-dynamics as well as brain metabolism. In particular, here NIRS has been applied in human volunteers as this methodology is based upon the use of harmless radiations so that to provide a non-invasive, non-ionizing procedure to monitor 2 main forms of hae­moglobin: oxy-haemoglobin (HbO2) and deoxy-haemoglobin (Hb). The data gathered indicate an overall positive influence of nicotine upon HbO2 levels, as well as total blood volume (V) therefore suggesting an increased brain metabolism. Finally these data further propose NIRS with its characteristics of noninvasiveness, easy to-use, portable, restraint-free therefore relatively psychologically undemanding, as replicable and ideal methodology for clinical applications and translational approaches.

Nicotine has a therapeutic window of effectiveness in a Drosophila melanogaster model of Parkinson’s disease

Strong epidemiological evidence and studies in models of Parkinson’s disease (PD) suggest that nicotine may be therapeutically beneficial in PD patients. However, a number of clinical trials utilizing nicotine in PD patients have had mixed results, indicating that either nicotine is not beneficial in PD patients, or an important aspect of nicotine therapy was absent. Here we show that continuous early nicotine administration improves both climbing and flight deficiencies present in homozygous park25 mutant PD model Drosophila melanogaster. Using a new climbing assay, we identify several climbing deficiencies in this PD model that are improved or rescued by nicotine treatment. Amongst these benefits, it appears that nicotine improves the ability of the park25 flies to descend the climbing vial by being able to climb down more. Importantly, we show that in order for nicotine benefits on climbing and flight to happen, nicotine administration must occur in a discrete time frame following adult fly eclosure: within one day for climbing or five days for flight. This therapeutic window of nicotine administration may help to explain its lack of efficacy in human clinical trials, suggesting a need to test earlier nicotine therapy in PD patients.

Effect of Nicotine Administration on Body Weight and Liver Enzymes in Male Rats

The study was conducted in Basrah University – veterinary medicine college, used about (60) sixty male rats divided into two groups randomly, control group and nicotine treated group with 0.5 mg / kg / BW, the result showed no significant difference in growth rats compared to control group also significant increase of liver enzymes compared to the control groups.

Progressive nicotine poisoning by multiple transdermal nicotine patches

The pharmacokinetic properties of transdermal nicotine patches (TNPs) are different from those of other routes of nicotine administration; further, acute nicotine poisoning by TNPs may present with different clinical features. In the present report, we describe the case of a 23-year-old woman who was admitted to emergency department (ED) at Jeju National University Hospital with loss of consciousness. Five hours before the ED visit, she used multiple TNPs to attempt suicide. Initially, nausea and vomiting occurred, and the symptoms worsened over time. We immediately removed the TNPs, and the application sites were gently washed with sterile water. The patient’s level of consciousness gradually improved, and she fully recovered an altered mental status 5 hours later. Her initial urinary cotinine level was 324 ng/mL. Physicians should be aware that acute nicotine poisoning by TNPs can cause various toxic symptoms.