Oral cancer is one of the ten leading cancers of the world. In India, it is one of the common cancers and is an important public health problem. Tobacco plays significant role in etiology of oral squamous carcinoma. Tobacco which is chewed or smoked contains many alkaloids which are known carcinogens. Oral submucous fibrosis (OSMF) is a disease of the Indian subcontinent, which through immigration has a worldwide distribution. Betel nut chewing plays significant role in etiology of OSMF. The nut alkaloids have been shown experimentally to result in stimulation of collagen synthesis by fibroblasts in vitro, which can induce precancerous conditions.Materials and Methods:The present study was undertaken to detect nitrate and nitrite factor in saliva of cases with oral carcinoma, OSMF and normal individuals without any habits and to determine whether increased salivary nitrate and nitrite level is significant in oral carcinoma and submucous fibrosis using biochemical parameters.Conclusion:We conclude that the major inducer of oral squamous cell carcinoma (OSCC) is exposure to tobacco. Recent studies have demonstrated that oxidative and nitrosative stress contributes to the development of oral carcinogenesis through deoxyribonucleic acid (DNA) damage. Salivary composition of OSCC patients is substantially altered with respect to free radical-involved mechanisms.

Streptozotocin diabetic male albino rats were observed to exhibit faulty conversion of tryptophan into niacin. Streptozotocininjected rats, kept on niacin-deficient diet and given a dose of Ltryptophan (intraperitoneal or oral) excreted comparatively less quantities of niacin and N'-methylnicotinamide in urine than the control nondiabetic rats. Rats continued to show this effect for at least three months after streptozotocin injection. Dietary intake was found to have no influence on the excretory pattern. Streptozotocin diabetic rats were also observed to excrete greater amounts of xanthurenic acid and other tryptophan metabolites on tryptophan administration as compared to the nondiabetic rats. DIABETES23:977-81, December, 1974.Diabetic condition has been observed by several workers to be accompanied by disturbed tryptophanniacin metabolism. Kotake and Tani 1 observed xanthurenic acid and 3-hydroxykynurenine in the urine of diabetic patients. Rosen et al. 2 reported increased urinary xanthurenic acid in diabetic patients following an oral dose of tryptophan indicating an impaired tryptophan-niacin metabolism. McDaniel et al. 3 have observed decreased N^methylnicotinamide (NMN) after tryptophan administration (oral or intraperitoneal route) in alloxan diabetic rats as compared to normal rats. Similar observations were reported by Ginoulhiac and coworkers 4 in pancreatectomized rats. Acetoacetate induced hyperglycemic rats were reported by Shastri and Nath 5 6 to exhibit • disturbed tryptophan metabolism.Streptozotocin,* a broad spectrum antibiotic, has been found to be strongly diabetogenic and is being increasingly used in inducing diabetes in experimental animals. Lower values of pyridine nucleotides in mouse liver 7 and rat pancreas 8 have been recently reported. In view of these reports investigations were undertaken to study the tryptophan-niacin metabolism in rats made diabetic by streptozotocin. MATERIALS AND METHODSMale albino rats (Wistar strain) about 200 gm. body weight were used in the present investigations. Streptozotocin* was dissolved in citrate buffer of pH 4.3 and was immediately injected intravenously at the level of 50 mg. per kilogram body weight. The control rats were injected with an equivalent volume of saline.Some of the rats were kept on the stock laboratory diet and some were fed a niacin-deficient diet. The composition of both the diets is indicated in table 1. After two weeks, niacin-deficient rats were transferred to metabolic cages and their basal urinary excretions of niacin and NMN were determined. They were then given L-tryptophan, niacin and niaeinamide at the levels indicated in table 2 and urinary excretion of niacin and NMN during the following twenty-four hours were estimated.For the estimation of niacin and NMN, urine samples were collected under toluene and glacial acetic acid. For xanthurenic acid and other metabolites, they were collected under toluene. Niacin was estimated by the cyanogen bromide method of Swaminathan 9 and NMN was determined by the fluorometric proced...

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SummaryBiosynthesis of niacin from 3-hydroxyanthranilic acid (3-OHAA) in normal and streptozotocin diabetic rats was studied in vivo and in vitro. Streptozotocin (SZ) diabetic rats were found to excrete lesser quantities of 3-OHAA, quinolinic acid, niacin and N1-methyl nicotinamide (NMN) in their urines following 3-OHAA administration than corresponding normal rats. In vitro studies indicated that SZ diabetic livers form less quinolinic acid from 3-OHAA than normal livers. It appears that this may be due to elevated picolinic carboxylase activity in the livers of SZ diabetic rats.Biosynthesis of niacin from tryptophan has been found to be affected in diabetic conditions, clinical (1, 2) as well as experimental (3, 4). The present authors recently reported that SZ-diabetic rats also exhibit faulty conversion of tryptophan into niacin; such rats were observed to excrete lesser quantities of niacin and NMN in their urines following tryptophan administration than the corresponding nondiabetic normal rats (5). SZ-diabetic rats have also been found to excrete comparatively larger quantities of kynurenine, 3-hydroxykynurenine and xanthurenic acid on tryptophan load as compared to the normal nondiabetic rats (6). In view of these observations, it was thought worthwhile to study the effects of suitable intermediates of tryptophan-niacin metabolism on niacin bio synthesis, both in vivo and in vitro with a view to pinpoint the site of the metabolic lesion. Of the three important intermediates-kynurenine, 3-OHAA and 3 -hydroxykynurenine, only 3-OHAA has been found to be useful in both, in vivo and in vitro, studies. Kynurenine and 3-hydroxykynurenine do not give rise to appreciable quantities of niacin in vitro under the conditions described in this communication. Only 3-OHAA under in vitro conditions is effectively converted into quinolinic acid, which can be converted into niacin by treatment with glacial