The Effect of Nicotine and its Interaction with Ethanol on Biochemical Parameters, Oxidative Damage and Histological Changes in the Rat’s Liver

Dhouib, Hanène; Jallouli, Manel; Draief, Monia; El-Fazaâ, Saloua; Bouraoui, Saâdia

doi:10.9790/2402-08157282

Cited by 10 publications

(9 citation statements)

References 61 publications

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“…This result is supported by previous studies reporting that tobacco caused hepatic damage both in vitro and in vivo due to oxidative stress associated with lipid peroxidation [45] [46] through induction of cytochrome P-450 [47]. In agreement with us, another study reported elevation of MDA in liver tissues-induced by nicotine and aggravated by ethanol [21]. Our results also revealed that co-exposure to nicotine and vitamin C caused significant reduction in the levels of MDA.…”

Section: Discussionsupporting

confidence: 82%

“…caused significant reduction in the total body weight, relative liver and kidney weights. The reduction in liver weight is supported by a previous study showing decreased liver weight in nicotine treated rats [21]. The reduction in body weight is supported by previous studies that reported lower body weight among smokers compared to non-smokers and weight gain in most subjects who quit smoking [22] [23] [24].…”

Section: Discussionsupporting

confidence: 77%

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Protective Effects of Vitamin C against Nicotine-Induced Oxidative Damage of Rat Liver and Kidney

Mahmoud¹

2014

IOSRJESTFT

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Abstract:Objective: Vitamin Methods: Animals were divided into four groups; (C) saline-treated, (VC) vitamin C-treated, (NIC) nicotinetreated, all were for 3 weeks, and (NIC+VC) is given vitamin C for 3 days prior, with nicotine injection and 2 days thereafter. Results: Present work showed that nicotine exposure caused significant reduction in total body weight, relative liver and kidney weights, elevated malondialdehyde (MDA), alanine transaminase (ALT), aspirate transaminase (AST), and alkaline phosphatase (ALP) in both hepatic and renal tissues. Co-exposure to nicotine and vitamin C maintained normal liver and kidney weight, significantly lowered MDA, ALT, AST, ALP and elevated glutathione in both hepatic and renal tissues compared NIC group as well as controls. Nicotine administration resulted in shedding, necrosis, and loss of brush border of cells covering proximal and distal convoluted tubules of kidney. The liver in the nicotine-treated group showed vacuolated cytoplasm of hepatocytes, with dilated central vein and sinusoids and mitochondrial destruction. Immunohistochemistry showed dense PCNA immunostaining in the livers of nicotine-treated rats. Vitamin C induced partial correction of nicotine-induced histopathological damage of liver and kidney and significant elevation in PCNA expression. Conclusion:The results of present work suggested that vitamin C has a promising prophylactic effect against nicotine-induced oxidative damage of liver and kidney.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionsupporting

confidence: 77%

Protective Effects of Vitamin C against Nicotine-Induced Oxidative Damage of Rat Liver and Kidney

Mahmoud¹

2014

IOSRJESTFT

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“…Moreover, rats exposed to both substances displayed higher levels of AST and alkaline phosphatase compared to those exposed to either substance alone ( p < .05). These findings align with a previous study that demonstrated increased AST, ALT and alkaline phosphatase in rats exposed to combined ethanol and nicotine exposure (Dhouib et al., 2014). AST, ALT and alkaline phosphatase are liver function enzymes that are typically present in the blood at low levels, and their elevated proportions indicate hepatocellular disease.…”

Section: Discussionsupporting

confidence: 93%

“…Alcohol consumption is well‐known to cause liver damage by stimulating excessive fatty acid production and accumulation, leading to various stages of liver inflammation (Lieber, 2004). However, the chronic consumption of nicotine can also affect liver function, as nicotine is primarily metabolized by the liver (Dhouib et al., 2014; Jensen et al., 2012). Nicotine binds to receptors located on the membranes of liver cells, activating a signalling pathway that induces an inflammatory process (Soeda et al., 2012).…”

Section: Discussionmentioning

confidence: 99%

Chronic alcohol and nicotine consumption as catalyst for systemic inflammatory storm and bone destruction in apical periodontitis

Pinto,

Fidalgo,

de Lima

et al. 2023

Int Endodontic J

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AimTo assess the periapical alveolar bone pattern and the serum levels of proinflammatory cytokines, biochemical markers and metabolites in rats subjected to chronic alcohol and nicotine consumption and induced apical periodontitis.MethodologyTwenty‐eight male Wistar rats were divided into four groups: Control, Alcohol, Nicotine and Alcohol+Nicotine. The alcohol groups were exposed to self‐administration of a 25% alcohol solution, while the other groups were given only filtered water. The nicotine groups received daily intraperitoneal injections of a nicotine solution (0.19 μL of nicotine/mL), whereas the other groups received saline solution. Periapical lesions were induced by exposing the pulps of the left mandibular first molars for 28 days. After euthanasia, the mandibles were removed and the percentage bone volume, bone mineral density, trabecular thickness, trabecular separation and trabecular number of the periapical bone were measured using micro‐computed tomography images. Serum samples were collected for analysis of proinflammatory cytokines (IL‐1β, IL‐4, IL‐6 and TNF‐α), biochemical and metabolomic analysis. Statistical analysis was performed with a significance level of 5%. Nonparametric data were analysed using the Kruskal‐Wallis test followed by Dunn's test, while one‐way anova followed by Tukey's test was performed for parametric data.ResultsThe groups exposed to alcohol or nicotine consumption exhibited an altered bone pattern indicating lower bone density and higher levels of IL‐1β, IL‐6 and TNF‐α compared to the Control group (p < .05). Significant differences were observed among the groups in the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase, cholesterol, triglycerides, urea, creatinine, albumin, uric acid, bilirubin and calcium. Metabolomic analysis revealed significant differences in glycine, phosphocholine, lysine, lactate, valine, pyruvate and lipids (CH2CH2CO), n(CH2) and n(CH3). Most of these parameters were even more altered in the simultaneous consumption of both substances compared to single consumption.ConclusionAlcohol and nicotine chronic consumption altered several metabolic markers, impaired liver and kidney function, increased the production of systemic proinflammatory mediators and harmed the periapical bone microarchitecture in the presence of apical periodontitis. The simultaneous consumption of alcohol and nicotine intensified these detrimental effects.

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“…Since increased LPO disrupts the normal function or destroys erythrocyte membranes and causes a leakage of the cytoplasmic marker such as LDH (indicator of cell and tissue damage) into circulation (30), we expected to find elevated values of this parameter as well as enhanced activity of AST and ALT, based on earlier findings in blood and various organs (14,29,(31)(32)(33)(34). Indeed, treatment with nicotine significantly increased LDH levels and the activities of ALT, AST compared to control (Table 1).…”

Section: Biochemical Test Resultsmentioning

confidence: 99%

Protective effects of quercetin and vitamin C against nicotine-induced toxicity in the blood of Wistar rats

Paunović

Ognjanović

Matić

et al. 2016

Archives of Industrial Hygiene and Toxicology

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Nicotine is a potential inducer of oxidative stress, through which it can damage numerous biological molecules. The aim of our study was to investigate the prooxidative effects of nicotine and protective (additive or synergistic) effects of quercetin and vitamin C in the blood of experimental animals, to determine whether the combination of these antioxidants might be beneficial for clinical purposes. Wistar albino rats were receiving intraperitoneal nicotine injection (0.75 mg kg -1 per day) or saline (control group) or nicotine plus quercetin (40 mg kg -1 per day) and vitamin C (100 mg kg -1 per day) for three consecutive days. On day 4, we determined their blood lipid profile, liver enzymes, oxidative stress parameters, and antioxidative system parameters. Compared to untreated control, nicotine significantly increased total cholesterol, LDLcholesterol, triglycerides, liver enzymes (alanine transaminase, aspartate transaminase, and lactate dehydrogenase) and oxidative stress parameters (superoxide anion, hydrogen peroxide, and lipid peroxide) and decreased HDL-cholesterol, glutathione, and superoxide dismutase/catalase activity. Quercetin + vitamin C reversed these values significantly compared to the nicotine alone group. Our results confirm that nicotine has significant prooxidative effects that may disrupt the redox balance and show that the quercetin + vitamin C combination supports antioxidant defence mechanisms with strong haematoprotective activity against nicotine-induced toxicity. In practical terms, this means that a diet rich in vitamin C and quercetin could prevent nicotine-induced toxicity and could also be useful in the supportive care of people exposed to nicotine.

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The Effect of Nicotine and its Interaction with Ethanol on Biochemical Parameters, Oxidative Damage and Histological Changes in the Rat’s Liver

Cited by 10 publications

References 61 publications

Protective Effects of Vitamin C against Nicotine-Induced Oxidative Damage of Rat Liver and Kidney

Protective Effects of Vitamin C against Nicotine-Induced Oxidative Damage of Rat Liver and Kidney

Chronic alcohol and nicotine consumption as catalyst for systemic inflammatory storm and bone destruction in apical periodontitis

Protective effects of quercetin and vitamin C against nicotine-induced toxicity in the blood of Wistar rats

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