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T C Tso

Publications and source records attributed to T C Tso.

At least 19 recordsLinked to original sources
PubMed1985

Clearance of polonium-210-enriched cigarette smoke from the rat trachea and lung.

The distribution and clearance of alpha radioactivity in the lungs of rats were measured after inhalation of smoke from cigarettes highly enriched in 210Po. Female Fischer rats were exposed daily for 6 months to smoke from cigarettes with 500 times the normal content of 210Po. Control rats were exposed to standard cigarette smoke. Animals were serially withdrawn and killed. After necropsy the trachea, major bronchi, larynx, and nasopharynx were examined for surface alpha activity by an etched track technique utilizing cellulose nitrate detectors. Areas of accumulated activity were seen on samples of larynx from rats exposed to the 210Po-enriched cigarettes. No other local accumulations were seen on the airways. The lower lungs were analyzed radiochemically for 210Po. Both radiochemical analysis and track measurements showed highly elevated activity concentrations in rats exposed to the 210Po-enriched cigarettes. Following withdrawal from smoking, both short- and long-term clearance components were seen. The parameters which fit the postexposure data for clearance of the lung burden cannot fit the buildup during the exposure period.

Animals↗
PubMed1978

Tobacco-specific nitrosamines: formation from nicotine in vitro and during tobacco curing and carcinogenicity in strain A mice.

The formation of tobacco-specific nitrosamines from the major tobacco alkaloid nicotine was examined. Detached leaf tobacco was fed either [2'-14C]nicotine or [2'-14C]nornicotine and air cured. The cured leaf was then analyzed for [2'-14C]N'-nitrosonornicotine ([2'-14C]NNN). The yield of [2'-14C]NNN was 0.007% from nornicotine and 0.009% from nicotine. Because the ratio of nicotine to nornicotine in conventional nicotine-type tobacco is 20-100:1, nicotine is considered to be the major precursor for the carcinogen NNN in tobacco. The formation of other nitrosamines from nicotine in vitro was then studied. Reaction of nicotine with NaNO2 gave rise to NNN, as well as to two other nitrosamines, 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and 4-(N-methyl-N-nitrosamino)-4-(3-pyridyl)butanal (NNA). Analysis of market products revealed the presence of NNK (0.6-24 microgram/g) in chewing tobacco and snuff. The tumorigenic activity of NNN, NNK, and NNA in strain A mice was studied. NNK induced more lung adenomas per mouse than did NNN, whereas NNA was less active than NNN. In addition, two cases of undifferentiated carcinoma of the salivary glands occurred in the NNN experimental groups.

Adenoma↗
PubMed1978

Chemical studies on tobacco smoke LVI. Tobacco specific nitrosamines: origins, carcinogenicity and metabolism.

Tobacco contains specific carcinogenic nitrosamines which are derived from nicotine. These compounds may be among the causative agents for the various cancers (lung, oral cavity, oesophagus, bladder and pancreas) which are associated with tobacco usage. The major tobacco specific nitrosamine is N'-nitrosonornicotine (NNN), which has been detected in both unburned tobacco (0.3-90.6 ppm) and cigarette mainstream smoke (137-238 ng/cig.). Studies with labelled precursors showed that the major source of NNN formed during curing of tobacco was nicotine, rather than nornicotine. The transfer rate of NNN from tobacco to mainstream smoke was 11.3%; about half the NNN present in smoke therefore originated from tobacco, with the remainder being formed during smoking. Model studies of the reaction of nicotine and nitrite showed that, in addition to NNN, two other nitrosamines, 4-(N-methyl-N-nitrosamino)-4-(3-pyridyl)-1-butanal (NNA) and 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) were formed. Analysis of tobacco revealed the presence of NNK in chewing tobacco and snuff (0.6-2.4 ppm). A comparative bioassay of NNN, NNK and NNA in strain A mice indicated that NNK was more tumorigenic than NNN and that NNA was inactive. NNN, which had previously been shown to induce oesophageal and nasal cavity tumours in rats, also was a moderately active carcinogen in the Syrian golden hamster, giving tracheal tumours. A study of the metabolism of cyclic nitrosamines was initiated. Metabolic alpha-hydroxylation of nitrosopyrrolidine, which is thought to be the critical step in activation of this compound, was demonstrated by detection in vitro and in vivo of 2-hydroxytetrahydrofuran, which was the product of decomposition of alpha-hydroxynitrosopyrrolidine. The metabolism of the related cyclic nitrosamine, NNN, is currently under investigation, with emphasis on metabolites resulting from alpha- and beta-hydroxylation. These analytical and metabolic studies are intended to clarify the possible relationship of tobacco-specific nitrosamines and site-specific cancers in tobacco users.

Anabasine↗
PubMed1976

Chemical studies on tobacco smoke. XLII. Nitrosonornicotine: presence in tobacco, formation and carcinogenicity.

NNN is the first organic carcinogen isolated from unburned tobacco. It has been found in smoking tobaccos, chewing tobaccos and in snuff in concentrations between 0.3 and 90.0 mug. This appears to be an unusually high concentration for a nitrosamine in an environmental agent. We have presented data which suggest that NNN, and possibly other unknown nitrosamines, are formed during the curing of tobacco and that the nitrate content of tobacco is an important factor in nitrosamine formation. Studies with N'-methylanabasine applied to tobacco plants are currently under way to test the idea that nicotine rather than nornicotine is the major precursor of NNN in processed tobacco. In mice, NNN induces adenomas of the lung. Bioassays with rats have shown that NNN is carcinogenic to the oesophagus and the nasal cavity. These chemical and biological data are consistent with the observation that tobacco chewers face an increased risk of cancer of the oesophagus. This observation does not, of course, rule out the possibility that other tobacco carcinogens are responsible for the increased cancer risk of tobacco chewers.

Animals↗
PubMed1973

Effects of some rare elements on nicotine content of the tobacco plant.

Fifty-four rare elements were tested for their effects on the nicotine level of tobacco (Nicotiana tabacum L.) plants grown in solution culture. Be, Cu, Pd, Pt, and Sm definitely increased nicotine yield (over 25%), whereas Bi, Co, Ho, Pb, Ni, Rb, Ag, Tl, Sn, U. V. and Zr definitely decreased nicotine yield. Cs, Er, Li, Rh, Ru, Se, Sr, Ti, and Yb possibly increased (less than 25%) nicotine yield, whereas As, Ce, Cr, Dy, Gd, I, Mo, Nd, Re, Ta, and Th possibly decreased nicotine yield. Other elements including Al, Ge, Au, Hf, In, Ir, La, Lu, Hg, Os, Pr, Sc, Te, Tb, Tm, W, and Zn showed no significant effects.

Journal Article↗
PubMed1970

Effect of photoperiod and end-of-day light quality on alkaloids and phenolic compounds of tobacco.

Tobacco plants (Nicotiana tabacum L.) were grown on long or short photoperiods followed by 5 minutes of red or far red radiation each day. Plants that received 16-hour photoperiods had a significantly higher concentration of total alkaloids and total phenolics than those that received 8-hour photoperiods. Significantly higher total alkaloid content was found in plants that received red rather than far red radiation last each day. Within each photoperiod, plants that received far red had higher concentrations of soluble phenols, particularly of chlorogenic acid. The interactions among these variables upon alkaloid and phenolic contents are discussed.

Alkaloids↗
PubMed1968

Fatty Acid composition in tobacco I. Green tobacco plants.

The major fatty acids (16 and 18 carbons) in leaves, flowers, and seeds of Nicotiana tabacum L. cv. Catterton have been analyzed at various intervals during the growth period. From the pattern of their accumulation and relative distribution, it was found that A) the amount of fatty acids in upper young leaves attained a maximum about 75 days after transplanting which is the time of early flowering, while in older leaves the fatty acids continuously declined; B) the relative amount of linolenic acid (18:3) increased progressively with leaf development, from 30% at an early stage to 60% at maturity, while other fatty acids (18:2, 18:1, 18:0, and 16:0) decreased during the same period, indicating a progressive desaturation; and C) a rapid increase of fatty acids was found as flowers developed into seedpods, particularly of linoleic acid (18:2), which comprises 75% of tobacco seed oil.Air-curing resulted in a loss of fatty acids, especially the unsaturated ones.

Journal Article↗
PubMed1966

Source of lead-210 and polonium-210 in tobacco.

Test plants were grown within a chamber enriched with radon-222 in the atmosphere, in tobacco fields with different sources of phosphate-containing fertilizer, and in culture containing lead-210 in the nutrient solution. Harvested leaves were subjected to three curing conditions. The major portion of the lead-210 in the plant was probably absorbed through the roots. Airborne radon 222 and its daughters contributed much less to the plant's content of lead-210 and of polonium-210. The stage of leaf development and the methods used to cure the leaf affected the final amount of polonium-210 in tobacco leaf.

Lead↗