Micronutrients and oxidative stress in the aetiology of cancer

Collins, Andrew; Duthie, Susan J.; Ross, Marion A.

doi:10.1079/pns19940011

Cited by 24 publications

(12 citation statements)

References 13 publications

(8 reference statements)

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“…The involvement of free radical-induced lipid peroxidation and the role of antioxidants in carcinogenesis are well established [25]. The decreased susceptibility of 4NQ0-induced oral tumors to lipid peroxidation compared with the surrounding non-malignant tissue and oral mucosa from control animals appears to be related to cell proliferation.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of 4-Nitroquinoline-1-Oxide-Induced Oral Carcinogenesis by Plant Products.

Manoharan

Ramachandran

et al. 1996

J. Clin. Biochem. Nutr.

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SummaryThe modifying effects of naturally occurring plant products such as neem leaf and turmeric extracts on 4-nitroquinoline-l-oxide (4NQO)-induced oral carcinoma were investigated in male Wistar strain rats. All the animals painted with 4NQ0 on their cheek mucosa for 20 weeks developed oral neoplasms identified histologically as squamous cell carcinoma. The oral tumor tissue showed a decrease in lipid peroxidation with concomitant changes in antioxidant activity. In groups of animals painted with 4NQ0 and simultaneous oral administration of neem leaf and turmeric extract, respectively, no tumors were observed; and the lipid peroxidation and antioxidant levels showed a pattern similar to that of untreated controls. Thus, the anticarcinogenic effect of neem leaf and turmeric extract appears to be related to their antioxidant function.We envisage that measurement of lipid peroxidation and antioxidant status with histological changes could be used to biomonitor tumor progression and evaluate the therapeutic response.

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Section: Discussionmentioning

confidence: 99%

Inhibition of 4-Nitroquinoline-1-Oxide-Induced Oral Carcinogenesis by Plant Products.

Manoharan

Ramachandran

et al. 1996

J. Clin. Biochem. Nutr.

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“…Oropharyngeal (OP) cancer, which is usually squamous cell carcinoma, is the most common head and neck malignancy, having a worldwide incidence of over 300 000 new cases each year and accounting for 2 -4% of all new cancers (Bross and Coombes, 1976;McGinnis and Foege, 1993;Collins et al, 1994;Ko et al, 1995;Piyathilake et al, 1995;Zheng et al, 1997;Nagler et al, 1999;Lippman and Hong, 2001). The commonly accepted paradigm for cigarette smoke (CS)-induced OP cancer pathogenesis is based on the assumption that a constant and direct attack of various CS carcinogens causes widespread accumulating cellular and DNA aberrations in the OP mucosa eventually leading to malignant transformation and cancer development.…”

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confidence: 99%

Saliva – a pivotal player in the pathogenesis of oropharyngeal cancer

2004

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Oropharyngeal (OP) cancer, which is usually squamous cell carcinoma, is the most common head and neck malignancy and accounts for 2 -4% of all new cancers. It is primarily induced by exposure to tobacco. The paradigm of cigarette smoke (CS)-induced OP cancer's pathogenesis is based on the assumption that a constant direct attack of various CS carcinogens causes widespread accumulating cellular and DNA aberrations in the OP mucosal cells, in turn eventually resulting in malignant transformation. However, there is never a direct contact between CS and the OP mucosa. Saliva, bathing the mucosa from the oral cavity to the larynx, always intervenes, and CS must first interact with saliva before it reaches the mucosa. The current study investigated the role of saliva in the pathogenesis of OP cancer. A synergistic effect of CS and saliva on oral cancer cells was demonstrated. This synergism is based on the reaction between redox active metals in saliva and low reactive free radicals in CS, which results in the production of highly active hydroxyl free radicals. Thus, when exposed to CS, salivary behavior is reversed and the saliva loses its antioxidant capacity and becomes a potent prooxidant milieu. The devastating role of CS-borne aldehydes was demonstrated as well. Based on these results and on our recent reports demonstrating that CS destroys various salivary components, including protective ones such as peroxidase, the most important salivary antioxidant enzyme, a comprehensive view of the pivotal role of saliva in the pathogenesis of CS-induced OP cancer is suggested. Oropharyngeal (OP) cancer, which is usually squamous cell carcinoma, is the most common head and neck malignancy, having a worldwide incidence of over 300 000 new cases each year and accounting for 2 -4% of all new cancers (Bross and Coombes, 1976;McGinnis and Foege, 1993;Collins et al, 1994;Ko et al, 1995;Piyathilake et al, 1995;Zheng et al, 1997;Nagler et al, 1999; Lippman and Hong, 2001). The commonly accepted paradigm for cigarette smoke (CS)-induced OP cancer pathogenesis is based on the assumption that a constant and direct attack of various CS carcinogens causes widespread accumulating cellular and DNA aberrations in the OP mucosa eventually leading to malignant transformation and cancer development. The CS-borne carcinogens are often thought to be free radicals. The process is initially expressed by dysplastic mucosal lesions which are then transformed into in situ carcinoma lesions, eventually resulting in fullblown infiltrating and metastasising OP cancer (Holleb et al, 1991). Chen et al (2002) demonstrated that chewing tobacco (areca quid) resulted in the formation of ROS in the oral cavity causing oxidative DNA damage to the surrounding tissues. Further support can be found in a report demonstrating that premalignant mucosal lesions and low-grade carcinomas express DNA aberrations following a pathway of exposure to free radicals (Sudb et al, 2001). Moreover, Bloching et al (2001) recently found increased genotoxic activity in the saliv...

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“…Tobacco (smoking and smokeless) use and excessive consumption of alcohol have been suggested as the main risk factors for oral and pharyngeal cancers, and perhaps for as much as 75% of these cancers (Toal, 1992;Collins et al, 1994). In the last three decades, the conspicuous international variations in cancer incidence and mortality, as well as observations in migrant populations, have raised the possibility that diet could be an important etiologic factor in carcinogenesis (Miller, 1985).…”

Section: Risk Factors For Oral Cancermentioning

confidence: 99%

“…Most studies link causation of oral cancer mainly to abuse of alcohol and tobacco (smoking and smokeless) (Toal, 1992;Collins et al, 1994). Implicit in this link but often ignored by investigators are the compounding roles of nutritional factors.…”

Section: General Commentsmentioning

confidence: 99%

Bionutrition and Oral Cancer in Humans

Enwonwu

Meeks

1995

Critical Reviews in Oral Biology & Medicine

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Tobacco (smoking and smokeless) use and excessive consumption of alcohol are considered the main risk factors for oral cancer . Conspicuous national and international variations in oral cancer incidence and mortality rates, as well as observations in migrant populations, raise the possibility that diet and nutritional status could be an important etiologic factor in oral carcinogenesis. As shown in this report, abuse of alcohol and tobacco has serious nutritional implications for the host, and generates increased production of reactive free radicals as well as eliciting immunosuppression. Maintenance of optimal competence of the immune system is critical for cancer surveillance. Active oxygen species and other reactive free radicals mediate phenotypic and genotypic alterations that lead from mutation to neoplasia. Consequently, the most widely used chemopreventive agents against oral cancer (e.g., vitamins A, E, C, and p-carotene) are anti-oxidants/free radical scavengers. These anti-oxidants, both natural and synthetic, neutralize metabolic products (including reactive oxygen species), interfere with activation of procarcinogens, prevent binding of carcinogens to DNA, inhibit chromosome aberrations, restrain replication of the transformed cell, suppress actions of cancer promoters, and may even induce regression of precancerous oral lesions such as leukoplakia and erythroplakia. Malnutrition is characterized by marked tissue depletion of anti-oxidant nutrients, including GSH (y-glutamyl-cysteinyl-glycine), a key cellular anti-oxidant as well as a modulator of T-cell activation. GSH or its precursor cysteine inhibits activation of the nuclear transcription factor kB (NFkB), and has been shown to be protective against chemically induced oral cancer and leukoplakia. Alcohol-, tobacco-, and/or malnutrition-induced immunosuppression promotes impaired salivary gland function and oral mucosal immunity, a prominent reduction in the number of helper CD4 cells with less marked changes in number of suppressor T-cells, and depressed NK cell activity, among others. These suggest a breakdown in the capacity of the malnourished to mount effective tumor surveillance. This review article underscores the compounding but important roles of nutritional/dietary factors in the long-established causal link between abuse of alcohol and tobacco (smoking and smokeless) and oral cancer.

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Micronutrients and oxidative stress in the aetiology of cancer

Cited by 24 publications

References 13 publications

Inhibition of 4-Nitroquinoline-1-Oxide-Induced Oral Carcinogenesis by Plant Products.

Inhibition of 4-Nitroquinoline-1-Oxide-Induced Oral Carcinogenesis by Plant Products.

Saliva – a pivotal player in the pathogenesis of oropharyngeal cancer

Bionutrition and Oral Cancer in Humans

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