Protective action of ascorbic acid and sulfur compounds against acetaldehyde toxicity: Implications in alcoholism and smoking

Sprince, Herbert; Parker, Clarence M.; Smith, George Gilbert; Gonzales, Leon J.

doi:10.1007/bf02027359

Cited by 57 publications

(40 citation statements)

References 49 publications

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“…Similar changes were also observed in the young ones. Studies have shown that Nacetylcysteine is an effective antidote for cyclophosphamide (Nelson et al, 1973), isophosphamide (Kline et al, 1973), acetaldehyde (Sprince et al, 1975) poisoning and in conjugation with pyridoxine an antagonist to the hepatotoxic effect of carbontetrachloride. N-acetylcysteine is also a known antioxidant.…”

Section: Discussionmentioning

confidence: 97%

Adaptation of siblings of female rats given ethanol effect of N-acetyl-L-cysteine

1997

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Summary. Ethanol administration to female rats before and during pregnancy resulted in decreased number of litters and increased activities of serum GOT, GPT and ALP. The hepatotoxicity of ethanol was indicated by the histological alterations both in the mother and siblings. There was increased levels of tissue lipids in mother and litters born to alcoholic rats. The concentration of TBARS in the liver and kidney were significantly increased in alcohol treated rats and their litters. The activities of the anti-peroxidative enzymes SOD and CAT were decreased on alcohol treatment in female rats. The glutathione content in liver and kidney decreased significantly in litters born to alcoholic rats.We have observed that the treatment with N-acetylcysteine offers protection against the toxic effect of alcohol in female rats during pregnancy and litters born to them. In N-acetylcysteine treated rats the number of litters as well as the average birth weight were close to that of control animals. Nacetylcysteine decreases the activities of serum GOT, GPT and ALP in female rats. We have also observed decreased levels of tissue lipids in mother and litters born to alcoholic rats given N-acetylcysteine when compared to alcoholic rats. The levels of TBARS in liver, kidney were also decreased both in mother and litter born to alcohol + N-acetylcysteine, while the activities of SOD and CAT were increased in liver of alcoholic rats given N-acetylcysteine when compared to alcoholic rats. Histopathological studies also showed the protective effect of N-acetylcysteine in both mother and litter in liver and kidney against alcoholic induced toxicity.

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Section: Discussionmentioning

confidence: 97%

Adaptation of siblings of female rats given ethanol effect of N-acetyl-L-cysteine

1997

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“…15 In vitro, the addition of increasing amounts of cysteine progressively decreases the detectable content of acetaldehyde. 39 In animal studies, externally given thiols protect from the lethal effects of acetaldehyde. 40 Pretreatment with an oral dose of Lcysteine or N-acetyl-cysteine gave 80% or more survivors in rats compared to controls when acetaldehyde (LD90 dose) was administered by oral intubation.…”

Section: Discussionmentioning

confidence: 99%

“…40 Pretreatment with an oral dose of Lcysteine or N-acetyl-cysteine gave 80% or more survivors in rats compared to controls when acetaldehyde (LD90 dose) was administered by oral intubation. 39 Cysteine has also been reported to reverse the acetaldehyde-induced inhibition of several mitochondrial functions in vitro. 41 These effects were concluded to endue from the thiol group of cysteine, which traps the reactivity of acetaldehyde.…”

Section: Discussionmentioning

confidence: 99%

Removal of acetaldehyde from saliva by a slow‐release buccal tablet of L‐cysteine

Salaspuro

Hietala

Kaihovaara

et al. 2001

Intl Journal of Cancer

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High alcohol intake is an independent risk factor for upper gastrointestinal (GI)-tract cancers. There is increasing evidence that acetaldehyde, the first metabolite of ethanol, might be responsible for ethanol-associated carcinogenesis. Especially among Asian heavy drinkers with the ALDH2-deficiency gene, i.e., a genetic inability to remove acetaldehyde, the risk of digestive tract cancers is markedly increased. Local acetaldehyde production from ethanol either by oral microbes, mucosal cells or salivary glands is a plausible carcinogenic agent in the saliva. The aim of our study was to examine whether is it possible to bind carcinogenic acetaldehyde from saliva with L-cysteine, which is slowly released from a special buccal tablet. Nine healthy male volunteers took part in our study, and each subject served as his own control. A placebo or L-cysteine-containing tablet was fastened under the upper lip. Thereafter the volunteers ingested 0.8 g/kg of body weight of 10% (v/v) ethanol, and saliva samples were collected at 20 min intervals for 320 min. Salivary acetaldehyde and ethanol levels were analysed by headspace gas chromatography. The mean reduction of acetaldehyde concentration of the saliva with the L-cysteine tablet compared to placebo was 59% (CL 95% 43%, 76%). Area under the curve (AUC 0 -320min ) with the L-cysteine and placebo tablet were 54.3 ؎ 11 M ؋ hr and 162 ؎ 34.2 M ؋ hr (mean ؎ SEM), respectively (p ‫؍‬ 0.003). After alcohol intake, up to two-thirds of carcinogenic acetaldehyde can be removed from saliva with a slow-releasing buccal L-cysteine drug formulation. Thus, a buccal cysteine tablet could potentially be used to prevent upper GI-tract cancers, especially among high-risk individuals. © 2002 Wiley-Liss, Inc. Key words: acetaldehyde; L-cysteine; upper digestive tract; carcinogenesisAlcohol intake and tobacco smoking are the most important independent risk factors for upper digestive tract cancers. [1][2][3][4][5] Many of the compounds in the tobacco smoke are carcinogenic, but, in contrast, the tumour-promoting effects of alcohol drinking has so far been less well defined. Acetaldehyde, the first metabolite of ethanol, has been shown to be carcinogenic in animals and there exists strong evidence of its carcinogenic action also in man. 6,7 Asian heavy drinkers with a genetically deficient aldehyde dehydrogenase (ALDH2) enzyme do show a markedly increased risk for GI-tract cancers. 8 Our recent findings demonstrate that Asians with this mutant ALDH2 have 2-3 times higher salivary acetaldehyde levels after a moderate dose of ethanol than Asians with the normal ALDH2 enzyme. 7 When this observation is combined with the earlier epidemiologic data, our results provide strong evidence for the local carcinogenic action of acetaldehyde produced from alcohol in the saliva by either oral microbes or in the salivary glands.After absorption, ethanol is evenly distributed to the waterphase of the body, and ethanol concentration in the saliva equals that of the blood. 9 In addition to the tissue alcohol ...

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“…Cysteine, a nonessential amino acid, is able to eliminate the toxicity of acetaldehyde by reacting covalently with acetaldehyde to form stable 2-methylthiazolidine-4-carboxylic acid (17). In our previous studies, we have been able to bind acetaldehyde originated from ethanol metabolism with orally administered L-cysteine (18).…”

Section: Introductionmentioning

confidence: 99%

Eliminating Carcinogenic Acetaldehyde By Cysteine From Saliva During Smoking

Salaspuro

Hietala

Marvola

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Tobacco smoking is one of the strongest risk factors not only for lung cancer but also for cancers of the upper gastrointestinal tract. Acetaldehyde has been shown to dissolve into the saliva during smoking and to be a local carcinogen in the human upper digestive tract. Cysteine can bind to acetaldehyde and eliminate its toxicity. We developed a tablet that releases cysteine into the oral cavity during smoking and could therefore be a potential chemopreventive agent against toxicity of tobacco smoke. In this study, the efficacy of L-cysteine -containing tablets to reduce the carcinogenic acetaldehyde in the saliva during tobacco smoking was examined. Seven volunteers smoked five cigarettes. During every smoking period, each volunteer sucked a blinded tablet containing 0, 1.25, 2.5, 5, or 10 mg of L-cysteine. Acetaldehyde was analyzed from salivary samples gas chromatographically at 0, 5, and 10 minutes from the beginning of the smoking. All tablets containing L-cysteine reduced highly significantly the salivary acetaldehyde; 5 mg of L-cysteine was the minimum concentration to totally eliminate the acetaldehyde from saliva. The mean salivary acetaldehyde concentrations in samples collected immediately after smoking with 0, 1.25, 2.5, 5, or 10 mg of L-cysteine were 228 F 115In conclusion, carcinogenic acetaldehyde could be totally inactivated in the saliva during smoking by sucking tablet containing 5 mg of L-cysteine. Even a small reduction of the carcinogenicity of cigarette smoke could gain benefit at the population level. Hence, this finding warrants for further clinical trials for L-cysteine tablet in the prevention of upper digestive tract cancers in

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Protective action of ascorbic acid and sulfur compounds against acetaldehyde toxicity: Implications in alcoholism and smoking

Cited by 57 publications

References 49 publications

Adaptation of siblings of female rats given ethanol effect of N-acetyl-L-cysteine

Adaptation of siblings of female rats given ethanol effect of N-acetyl-L-cysteine

Removal of acetaldehyde from saliva by a slow‐release buccal tablet of L‐cysteine

Eliminating Carcinogenic Acetaldehyde By Cysteine From Saliva During Smoking

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