Protective Effects of Taurine against Nicotine-Induced Oxidative Damage of Rat Urinary Bladder and Kidney

Şener, Göksel; Şehirli, Özer; İpçi, Yeşim; Çetınel, Şule; Çikler, Esra; Gedik, Nursal; Ali̇can, İnci̇

doi:10.1159/000083245

Cited by 45 publications

(25 citation statements)

References 38 publications

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“…However, Arany et al (2011) found that chronic nicotine exposure increased the extent of renal injury which may be attributed to their prolonged treatment for 4 weeks. Similarly, measurement of BUN showed no significant changes which is in contrary to the finding of Sener et al (2005) who show a significant increase in the BUN values. Interestingly, nicotine by itself produced a less profound effect on BUN than to its combination treatment with alcohol (Bekairi et al 1987).…”

Section: B a D C Econtrasting

confidence: 93%

“…An insignificant rise in the plasma levels of the creatinine due to nicotine treatment was observed by us what is in line with the observation of other groups (Sener et al 2005). However, Arany et al (2011) found that chronic nicotine exposure increased the extent of renal injury which may be attributed to their prolonged treatment for 4 weeks.…”

Section: B a D C Esupporting

confidence: 90%

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Thromboembolic injury and systemic toxicity induced by nicotine in mice

Fahim

Al‐Salam²,

Dhanasekaran³

et al. 2014

gpb

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Abstract. Nicotine is involved in the pathogenesis of hematological and cardiopulmonary diseases. However, the understanding of the pathophysiological mechanisms underlying these undesirable effects is unclear. Cigarette smoking, nicotine gums and patches are common sources for nicotine ingestion. We have investigated the nicotine's effect on cerebral microvessel thrombosis and systemic toxicity. Mice received either nicotine (1 mg/kg, i.p.) or saline (control), once a day for 21 days. Briefly, after bolus intravenous fluorescein injection, a photo insult of cerebral microvessel was done. The platelet aggregation in microvessels was video recorded and analyzed. In conjunction, the plasma levels of superoxide dismutase (SOD), lactate dehydrogenase (LDH), liver enzymes, creatinine and blood urea nitrogen (BUN), and histopathological studies were carried out. Our results revealed a significant prothrombotic effect following nicotine exposure. Significant decrease in SOD indicates the occurrence of oxidative stress involved in the tissue damages and increase in the LDH emphasize the systemic toxicity. Substantial rise in the liver aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were observed. Lungs histology showed intra-vascular hemorrhagic infarction with necrosis, macrophage and neutrophils infiltration. Liver histology showed intravascular thrombosis and portal inflammation. We conclude that the sub-acute nicotine exposure causes an increase in thrombosis in cerebral microvessels and systemic, hepatic and pulmonary toxicity.

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Section: B a D C Econtrasting

confidence: 93%

Section: B a D C Esupporting

confidence: 90%

Thromboembolic injury and systemic toxicity induced by nicotine in mice

Fahim

Al‐Salam²,

Dhanasekaran³

et al. 2014

gpb

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“…Chronic NIC exposure increases ROS production in mesangial (23) and proximal tubule (25) cells in vitro. In animal models, chronic exposure to cigarette smoke or NIC significantly increased oxidative stress in the kidney and pretreatment with antioxidants prevented renal injury (9,22,32,43). These results clearly connect smoking/chronic NIC to oxidative injury.…”

Section: Discussionmentioning

confidence: 73%

“…19). Chronic exposure to NIC increases oxidative stress in the kidney (22,43), cultured proximal tubule (25), or mesangial cells (23), thus linking smoking and NIC to renal injury (23). Consequently, smoking or chronic NIC exposure might exacerbate acute renal injury through increasing oxidative stress as observed in experimental radiocontrast-induced AKI (17).…”

mentioning

confidence: 99%

Chronic nicotine exposure exacerbates acute renal ischemic injury

Arany¹,

Grifoni

Clark³

et al. 2011

American Journal of Physiology-Renal Physiology

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Recent epidemiological reports showed that smoking has a negative impact on renal function and elevates the renal risk not only in the renal patient but perhaps also in the healthy population. Studies suggested that nicotine, a major tobacco alkaloid, links smoking to renal dysfunction. While several studies showed that smoking/chronic nicotine exposure exacerbates the progression of chronic renal diseases, its impact on acute kidney injury is virtually unknown. Here, we studied the effects of chronic nicotine exposure on acute renal ischemic injury. We found that chronic nicotine exposure increased the extent of renal injury induced by warm ischemia-reperfusion as evidenced by morphological changes, increase in plasma creatinine level, and kidney injury molecule-1 expression. We also found that chronic nicotine exposure elevated markers of oxidative stress such as nitrotyrosine as well as malondialdehyde. Interestingly, chronic nicotine exposure alone increased oxidative stress and injury in the kidney without morphological alterations. Chronic nicotine treatment not only increased reactive oxygen species (ROS) production and injury but also exacerbated oxidative stress-induced ROS generation through NADPH oxidase and mitochondria in cultured renal proximal tubule cells. The resultant oxidative stress provoked injury through JNK-mediated activation of the activator protein (AP)-1 transcription factor in vitro. This mechanism might exist in vivo as phosphorylation of JNK and its downstream target c-jun, a component of the AP-1 transcription factor, is elevated in the ischemic kidneys exposed to chronic nicotine. Our results imply that smoking may sensitize the kidney to ischemic insults and perhaps facilitates progression of acute kidney injury to chronic kidney injury.

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“…Nicotine itself induces oxidant damage in various organs by increasing lipid peroxidation products and decreasing the activity of endogenous antioxidants [Sener et al 2005] and the higher levels of nicotine that the fetus is exposed to than the mother implies that the fetus is also exposed to higher levels of oxidants. This can readily result in an oxidant/antioxidant imbalance which can adversely impact on cell survival and thus development of organs.…”

Section: Nutrient Supplementationmentioning

confidence: 99%

Are nicotine replacement therapy, varenicline or bupropion options for pregnant mothers to quit smoking? Effects on the respiratory system of the offspring

Maritz

2009

Ther Adv Respir Dis

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Nicotine occurs in tobacco smoke. It is a habit-forming substance and is prescribed by health professionals to assist smokers to quit smoking. It is rapidly absorbed from the lungs of smokers. It crosses the placenta and accumulates in the developing fetus. Nicotine induces formation of oxygen radicals and at the same time also reduces the antioxidant capacity of the lungs. Nicotine and the oxidants cause point mutations in the DNA molecule thereby changing the program that controls lung growth and maintenance of lung structure. The data available indicate that maternal nicotine exposure induces a persistent inhibition of glycolysis and a drastically increased AMP level. These metabolic changes are thought to contribute to the faster aging of the lungs of the offspring of mothers that are exposed to nicotine via the placenta and mother's milk. The lungs of these animals are more susceptible to damage as shown by the gradual deterioration of the lung parenchyma. The rapid metabolic and structural aging of the lungs of the animals exposed to nicotine via the placenta and mother's milk, and thus during phases of lung development characterized by rapid cell division, is likely due to 'programming' induced by nicotine. Since varenicline, a partial nicotine agonist, has basically the same structure as nicotine, and also binds to acetylcholine receptors in competition with nicotine (but with largely the same effect), it is not advisable to use nicotine or varenicline during gestation and lactation. Furthermore, the use of individual vitamin supplements is also not advisable because of the negative impact on the program that controls maintenance of lung structural and functional integrity and aging. A more appropriate smoking cessation program will also include a mixture of antioxidant nutrients such as in tomato juice.

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Protective Effects of Taurine against Nicotine-Induced Oxidative Damage of Rat Urinary Bladder and Kidney

Cited by 45 publications

References 38 publications

Thromboembolic injury and systemic toxicity induced by nicotine in mice

Thromboembolic injury and systemic toxicity induced by nicotine in mice

Chronic nicotine exposure exacerbates acute renal ischemic injury

Are nicotine replacement therapy, varenicline or bupropion options for pregnant mothers to quit smoking? Effects on the respiratory system of the offspring

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