Role of green tea on nicotine toxicity on liver and lung of mice: Histological and morphometrical studies

Gawish, Azza M.; Issa, Aliaa M.; Bassily, Nahed S.; Manaa, Sherin M.

doi:10.5897/ajb11.141

Cited by 10 publications

(4 citation statements)

References 42 publications

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“…Nicotineinduced mice showed different histopathological changes including inflammatory cells, congested blood vessels, haemorrhage and degeneration of some hepatic cells. These observations were in harmony with the results of Gawish et al (2012). The damaging effect of nicotine on hepatic tissues has been previously reported (Salahshoor et al, 2016 andMunir et al, 2015).…”

Section: Resultssupporting

confidence: 91%

Ameliorative Effect of Teucrium polium Extract against Nicotine Induced Liver Toxicity in Swiss Albino Mice

Alatawi,

Alarifi,

Al-Shaebi

et al. 2024

IJAR

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Background: Nicotine can be consumed in many forms, the most common of which is smoking tobacco. Tobacco smoking is a global problem that negatively affects human health. Natural plants are vital antioxidants that may antagonize the toxic effects of smoking. We designed the present study to assess the protective potential of Teucrium polium extract (TPE) on nicotine-induced liver toxicity in male mice. Methods: Twenty-four animals were allocated into four equal groups and daily treated for 21 constitutive days. Control group one received distilled water, group two orally received 100 mg/kg TPE, group three received subcutaneous injections of 2.5 mg/kg nicotine and group four received 100 mg/kg TPE orally then 2.5 mg/kg nicotine subcutaneously after one hour. Result: Nicotine exposure significantly elevated liver enzymes; alanine transaminase (ALT) and aspartate transaminase (AST). The levels of malondialdehyde (MDA) and nitric oxide (NO) were also elevated along with a reduction in glutathione reduced content (GSH), superoxide dismutase (SOD) and catalase (CAT) activity. Treatment with TPE considerably ameliorated the serum levels of liver enzymes, lowered MDA and NO levels, as well as elevated the antioxidant defense system. Also, TPE improved the histological structure and modulated apoptosis caused by nicotine. The current study proved the effectiveness of TPE as a natural antioxidant for the alleviation of nicotine-induced hepatic biochemical and histopathological alterations through attenuating oxidative stress, improving antioxidant systems and abrogating apoptosis.

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Section: Resultssupporting

confidence: 91%

Ameliorative Effect of Teucrium polium Extract against Nicotine Induced Liver Toxicity in Swiss Albino Mice

Alatawi,

Alarifi,

Al-Shaebi

et al. 2024

IJAR

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“…The toxic effect of nicotine on mouse hepatocytes was reported in a similar study on Swiss albino mice. It has been suggested that nicotine has hepatotoxic effects due to hepatocyte accumulation of iron, increased pro-inflammatory cytokine levels, and reduced glutathione peroxidase activity and glutathione levels [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

Nicotine Exerts Cytotoxic Effects in a Panel of Healthy Cell Lines and Strong Irritating Potential on Blood Vessels

Chioran

Sitaru

Macaşoi

et al. 2022

IJERPH

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The use of tobacco products is a major global public health issue, as it is the leading cause of preventable death worldwide. In addition, nicotine (NIC) is a key component of electronic and conventional cigarettes. Although nicotine’s addictive potential is well known, its health effects are not entirely understood. Thus, the main objective of the present study was to evaluate its toxicological profile both in vitro, at the level of three healthy cell lines, and in ovo, at the level of the chorioallantoic membrane. Five different concentrations of nicotine were used in keratinocytes, cardiomyocytes, and hepatocytes for the purpose of evaluating cell viability, cell morphology, and its impact on nuclei. Additionally, the hen’s egg test on the chorioallantoic membrane (HET-CAM) method was used to assess the biocompatibility and irritant potential of the chorioallantoic membrane. Across all cell lines studied, nicotine was proven to be significantly damaging to cell viability, with the highest concentration tested resulting in less than 2% viable cells. Moreover, the morphology of cells changed dramatically, with alterations in their shape and confluence. Nicotine-induced cell death appears to be apoptotic, based on its impact on the nucleus. In addition, nicotine was also found to have a very strong irritating effect on the chorioallantoic membrane. In conclusion, nicotine has an extremely strong toxicological profile, as demonstrated by the drastic reduction of cell viability and the induction of morphological changes and nuclear alterations associated with cellular apoptosis. Additionally, the HET-CAM method led to the observation of a strong irritating effect associated with nicotine.

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“…14 In addition, nicotine is also rapidly absorbed into the circulatory system and metabolized through cytochrome P450 in the liver during smoking. 15 It is also suggested that nicotine may be genotoxic, because high doses of nicotine could significantly increase mutation frequency and sister chromatid exchange frequency in vitro. 16,17 Besides, Chen et al reported that nicotine could activate RPS27a-Mdm2-P53 and AKT/mTOR pathways, as well as 4EBP1/ eIF4E axis and its translational activity, leading to human papillomavirus (HPV)-immortalized cervical epithelial (H8) cell proliferation in cellular experiments.…”

Section: Introductionmentioning

confidence: 99%

“…Studies have found that it plays a key role in the progression and metastasis of certain cigarette-related cancers, such as stomach, lung, colon, and cervical cancer, as well as HCC . In addition, nicotine is also rapidly absorbed into the circulatory system and metabolized through cytochrome P450 in the liver during smoking . It is also suggested that nicotine may be genotoxic, because high doses of nicotine could significantly increase mutation frequency and sister chromatid exchange frequency in vitro. , Besides, Chen et al reported that nicotine could activate RPS27a-Mdm2-P53 and AKT/mTOR pathways, as well as 4EBP1/eIF4E axis and its translational activity, leading to human papillomavirus (HPV)-immortalized cervical epithelial (H8) cell proliferation in cellular experiments. , Furthermore, nicotine could form adducts with mouse liver DNA and lung DNA, as well as histone H1/H3, Hb, and albumin in mice .…”

Section: Introductionmentioning

confidence: 99%

Nicotine Promotes WRL68 Cells Proliferation Due to the Mutant p53 Gain-of-Function by Activating CDK6-p53-RS-PIN1-STAT1 Signaling Pathway

Huai

Chen²,

Zhou

et al. 2020

Chem. Res. Toxicol.

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The liver is an important organ with many tasks, such as dealing with drugs, alcohol and other toxins to remove them from the body. Nicotine is the more abundant component in cigarette smoking, which is first metabolized in liver and increases the risk of developing hepatocellular carcinoma (HCC). Also, genotoxic potential of nicotine has been extensively studied in vitro. However, the carcinogenic action of nicotine on the HCC needs to be elucidated. The current study demonstrated that chronic exposure to nicotine significantly promotes human normal fetal hepatic cell line (WRL68 cells) proliferation in a time- and concentration-dependent manner resulting from G0/G1-S-phase transition. Also remarkably, nicotine induced the level of p53 mutation at Ser249 (p53-RS). Note as well that the level of STAT1 protein was increased along with p53-RS owing to the prolonged half-life of STAT1. Furthermore, it is suggested that CDK6-dependent binding between phosphorylation of p53-RS at Ser249 and PIN1 by nicotine treatment leads to the nucleus translocation, followed by interacting with STAT1 and subsequent activation of STAT1 via the improvement of its stability, which is involved in cellular growth and colony formation after nicotine treatment. Simply put, these findings indicated that nicotine induces mutant p53 gain-of function (GOF), activating CDK6-p53-RS-PIN1-STAT1 signaling pathway and promoting cell proliferation, which could contribute to HCC for smokers.

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Role of green tea on nicotine toxicity on liver and lung of mice: Histological and morphometrical studies

Cited by 10 publications

References 42 publications

Ameliorative Effect of Teucrium polium Extract against Nicotine Induced Liver Toxicity in Swiss Albino Mice

Ameliorative Effect of Teucrium polium Extract against Nicotine Induced Liver Toxicity in Swiss Albino Mice

Nicotine Exerts Cytotoxic Effects in a Panel of Healthy Cell Lines and Strong Irritating Potential on Blood Vessels

Nicotine Promotes WRL68 Cells Proliferation Due to the Mutant p53 Gain-of-Function by Activating CDK6-p53-RS-PIN1-STAT1 Signaling Pathway

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