Vitamin C prevents cigarette smoke induced oxidative damage of proteins and increased proteolysis

Panda, Koustubh; Chattopadhyay, Ranajoy; Ghosh, Mrinal K.; Chattopadhyay, D.; Chatterjee, Indu B.

doi:10.1016/s0891-5849(99)00154-9

Cited by 75 publications

(75 citation statements)

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“…We had previously demonstrated that cigarette smoke (CS) can directly oxidize animal lung proteins both in vitro (2) and in vivo (3) and, thereby, render them susceptible to increased proteolytic damage consistent with that observed in CS-induced emphysema. However, we were then unable to identify the precise cellular factors involved in the damage process (3)(4)(5).…”

mentioning

confidence: 61%

“…Also, to examine possible involvement of CS and cell-generated oxidants besides NO, in the observed lung damage, we orally administered the CS-treated animals with ascorbate or vitamin C, an antioxidant with established capability of scavenging such oxidants de novo (2,33). Morphometric analysis of alveolar airspace expansion (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…However, this controversy seems to be finally waning with several carefully designed studies showing that ascorbate predominantly acts as a potent antioxidant in vivo (47). Indeed, the potential of vitamin C or ascorbate to prevent CSinduced lung damage has been first reported by us through in vitro (2,5) as well as in vivo (3) studies using guinea pig models of CSinduced emphysema. Thereafter, several other groups have vindicated our observations (26,48,49).…”

Section: Gupta Et Almentioning

confidence: 99%

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Ascorbate attenuates pulmonary emphysema by inhibiting tobacco smoke and Rtp801-triggered lung protein modification and proteolysis

Gupta

Ganguly

Rozanas³

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Cigarette smoking causes emphysema, a fatal disease involving extensive structural and functional damage of the lung. Using a guinea pig model and human lung cells, we show that oxidant(s) present in tobacco smoke not only cause direct oxidative damage of lung proteins, contributing to the major share of lung injury, but also activate Rtp801, a key proinflammatory cellular factor involved in tobacco smoke-induced lung damage. Rtp801 triggers nuclear factor κB and consequent inducible NOS (iNOS)-mediated overproduction of NO, which in combination with excess superoxide produced during Rtp801 activation, contribute to increased oxidonitrosative stress and lung protein nitration. However, lung-specific inhibition of iNOS with a iNOS-specific inhibitor, N6-(1-iminoethyl)-L-lysine, dihydrochloride (L-NIL) solely restricts lung protein nitration but fails to prevent or reverse the major tobacco smoke-induced oxidative lung injury. In comparison, the dietary antioxidant, ascorbate or vitamin C, can substantially prevent such damage by inhibiting both tobacco smoke-induced lung protein oxidation as well as activation of pulmonary Rtp801 and consequent iNOS/NO-induced nitration of lung proteins, that otherwise lead to increased proteolysis of such oxidized or nitrated proteins by endogenous lung proteases, resulting in emphysematous lung damage. Vitamin C also restricts the up-regulation of matrix-metalloproteinase-9, the major lung protease involved in the proteolysis of such modified lung proteins during tobacco smoke-induced emphysema. Overall, our findings implicate tobacco-smoke oxidant(s) as the primary etiopathogenic factor behind both the noncellular and cellular damage mechanisms governing emphysematous lung injury and demonstrate the potential of vitamin C to accomplish holistic prevention of such damage.cigarette smoke | emphysema | vitamin C | ascorbate | Rtp801

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mentioning

confidence: 61%

Section: Resultsmentioning

confidence: 99%

Section: Gupta Et Almentioning

confidence: 99%

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Ascorbate attenuates pulmonary emphysema by inhibiting tobacco smoke and Rtp801-triggered lung protein modification and proteolysis

Gupta

Ganguly

Rozanas³

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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“…Diet derived antioxidant vitamins B, C and E provide protection by reacting with radicals terminating oxidation cascades. Cigarette smoke depletes plasma concentrations of vitamin C, E and carotenoids (Chow et al 1986;Alberg 2002;Panda et al 1999;Bruno and Traber 2006) and supplementation of antioxidants inhibits cigarette smoke induced oxidative damage in vivo (Panda et al 2000).Acute cigarette smoke exposure also reduces the levels of endogenous circulating anti-oxidant molecules. Glutatione, cysteine, methylumbellifere glucuronide and ferrodxidase are all reduced in serum after smoke exposure (Moriarty et al 2003; Van der Vaart et al 2004).…”

Section: Systemic Antioxidant Mechanismsmentioning

confidence: 99%

The Pathophysiology of Cigarette Smoking and Age-Related Macular Degeneration

Dhubhghaill

Cahill

Campbell

et al. 2009

Advances in Experimental Medicine and Biology

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Age-related macular degeneration (AMD) is the most common form of visual impairment, in people over 65, in the Western world. AMD is a multifactorial disease with genetic and environmental factors influencing disease progression. Cigarette smoking is the most significant environmental influence with an estimated increase in risk of 2- to 4-fold. Smoke-induced damage in AMD is mediated through direct oxidation, depletion of antioxidant protection, immune system activation and atherosclerotic vascular changes. Moreover, cigarette smoke induces angiogenesis promoting choroidal neovascularisation and progression to neovascular AMD. Further investigation into the effects of cigarette smoke through in vitro and in vivo experimentation will provide a greater insight into the pathogenesis of age-related macular degeneration.

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“…This commitment stems of an increases aggregation of blood platelet, an important step in the genesis of atherosclerosis. Others malefi cent effects of passive smoke are the exposure to carcinogenic agents (ex: benzopyrene), increased production of reactive oxygen species (ROS) and necrosis of tissues 3,4 .…”

Section: Introductionmentioning

confidence: 99%

New experimental model of exposure to environmental tobacco smoke

Brito¹,

Yasojima²,

Silveira

et al. 2013

Acta Cir. Bras.

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PURPOSE:To describe a new model to passive smoking for rodents. METHODS:Twenty rats were distributed into two study groups (N=10): control group (CG), that was not exposed to tobacco smoke and used as normal standard for biochemical and histological analysis; Experimental Group (EG), that Animals were exposed to the passive smoking; Euthanasia was performed after 14 days of exposure. The serum level of nicotine and histological analysis were performed. RESULTS:There was a statistical difference on the nicotine serum levels between Experimental and Control group, with level of 286 ±23 nanograma/mL in the EG and undetectable on CG (p<0.01). The histological study suggested the model efficacy producing alveolar destruction and emphysema in the EG compared with the insignificant lesions in the CG`s lung. CONCLUSION:The model of exposure to environmental tobacco smoke for rodents induced easily the changes related to secondhand smoke.

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Vitamin C prevents cigarette smoke induced oxidative damage of proteins and increased proteolysis

Cited by 75 publications

References 53 publications

Ascorbate attenuates pulmonary emphysema by inhibiting tobacco smoke and Rtp801-triggered lung protein modification and proteolysis

Ascorbate attenuates pulmonary emphysema by inhibiting tobacco smoke and Rtp801-triggered lung protein modification and proteolysis

The Pathophysiology of Cigarette Smoking and Age-Related Macular Degeneration

New experimental model of exposure to environmental tobacco smoke

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