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PubMed1995

Urethane directly inhibits chemoreflex excitation of medullary vasomotor neurons in rats.

In anesthetized rats, stimulation of the arterial chemoreceptors excites reticulospinal vasomotor neurons of the nucleus rostroventrolateral reticularis of the medulla oblongata, via activating the neuronal NMDA receptors. Excitation of these neurons is responsible for reflex increases in sympathetic neuronal activity and arterial pressure. Additional doses (0.12-0.24 g/kg i.v.) of urethane dose-dependently reduced the elevations in the discharge rate of reticulospinal vasomotor and sympathetic neurons and of arterial pressure, elicited by stimulating the carotid chemoreceptors with intra-carotid injections of sodium cyanide (100 nmol/10 microl), without affecting discharges of the carotid chemoafferents. Microiontophoresis of urethane onto the reticulospinal vasomotor neurons reversibly inhibited the excitation elicited by stimulation of the chemoreceptors and by iontophoretically applied L-glutamate. The results indicate that the suppression of chemoreflexes by excessive amount of urethane is central and one of its blocking excitatory amino acid transmission onto these vasomotor neurons.

Anesthetics, Intravenous↗

PubMed2006

Effect of different Thai traditional processing of various hot chili peppers on urethane-induced somatic mutation and recombination in Drosophila melanogaster: assessment of the role of glutathione transferase activity.

Four different Thai traditional chili peppers, namely bird pepper (Capsicum frutescens), red chili spur peppers (Capsicum annuum), green bell peppers and sweet pepper (C. annuum) were investigated for their antimutagenic properties. Each chili was prepared in three formulations commonly used for chili food processing; raw paste (chili ground in water), pickled in vinegar or stir-fried in palm oil. Each sample was tested for its antimutagenic effect against urethane by using the somatic mutation and recombination of wing hair of Drosophila melanogaster as an indicator. Three-day-old larvae, trans-heterozygous for two genetic markers, multiple wing hairs mwh and orrigon (ORR;flr3), were exposed to urethane alone or in combination with each chili formulation. The various processing methods for chilies differentially extracted the antimutagenic chili components. The specific chili as well as the method of processing influenced the observed antimutagenic properties against urethane. This suggested each chili contains a unique complex mixture of many antimutagens. Co-treatment and pre-treatment experiments showed that both direct and indirect protective mechanisms are involved in an 'activation' process to give antimutagenesis effects. An association between antigenotoxicity and glutathione transferase activity could not be established.

Animals↗

PubMed2004

Cocaine-induced Fos expression in rat striatum is blocked by chloral hydrate or urethane.

Anesthetics used in electrophysiological studies alter the effects of cocaine and amphetamine on neural activity in the striatum. However, the mechanism underlying this alteration has not been established. In the present study, we examined the effects of anesthetics on cocaine-induced neural activity in the striatum. We first assayed the ability of 20 mg/kg cocaine to induce Fos expression in the striatum following pretreatment with 400 mg/kg chloral hydrate or 1.3 g/kg urethane, two of the most commonly used anesthetics for in vivo electrophysiology. Chloral hydrate blocked, while urethane strongly attenuated cocaine-induced Fos expression without affecting basal levels of expression. We then examined dopaminergic and glutamatergic mechanisms for anesthetic effects on cocaine-induced Fos expression. Chloral hydrate and urethane did not attenuate basal or cocaine-induced increases of dopamine levels as assessed by microdialysis in dorsal striatum. In contrast, chloral hydrate attenuated glutamatergic neurotransmission as assessed by microdialysis in the presence of the glutamate transport blocker L-trans-pyrrolidone-2,4-dicarboxylic acid. Chloral hydrate attenuated basal levels of glutamate by 70%, while cocaine had no effect on glutamate levels. Since glutamate levels were tetrodotoxin-sensitive, the majority of glutamate measured in our assay was by synaptic release. To assess a causal role for a reduction of glutamatergic neurotransmission in anesthetic effects on cocaine-induced Fos expression, we injected the glutamate receptor agonists AMPA and NMDA into the dorsal striatum of chloral hydrate-anesthetized rats. The glutamate receptor agonists partially reinstated cocaine-induced Fos expression in anesthetized rats. We conclude anesthetics attenuate cocaine-induced neuronal activity by reducing glutamatergic neurotransmission.

Amino Acid Transport System X-AG↗

PubMed2005

Gene expression analysis of urethane-induced lung tumors in ras H2 mice.

In our previous study, microarray analysis was performed on N-ethyl-N-nitrosourea (ENU)-induced forestomach tumors in transgenic mice carrying the human prototype c-Ha-ras gene (ras H2 mice). Ras-MAPK related genes, including the transgene and mouse endogenous ras genes, that are involved in enhanced carcinogenesis were up-regulated in these tumors. In the present study, ras H2 mice received five intraperitoneal injections of 1,000 mg/kg urethane at 2-day intervals. Subsequently, microarray and RT-PCR analyses for the transgene and some molecules involved in the Ras pathway were performed on the induced lung tumors. In the microarray analysis, gene expression profiles of normal lungs and adenomas showed a distinct pattern, and several genes related to the cell cycle and nucleotide metabolism were up-regulated in the adenomas. RT-PCR confirmed the overexpression of the transgene in lung tumors; however, the up-regulation of the mouse endogenous ras genes was not observed. Some genes showed a similar expression pattern in both ENU- and urethane-induced tumors. These results suggest that the overexpression of the transgene plays an important role in the carcinogenesis of both ENU- and urethane-induced tumors in ras H2 mice. The genes that showed a similar expression pattern in both tumors were considered to be the candidate genes responsible for enhanced carcinogenesis.

Adenoma↗

PubMed1994

Brain temperature- and behavior-related changes in the dentate gyrus field potential during sleep, cold water immersion, radiant heating, and urethane anesthesia.

The field potential evoked in the dentate gyrus (DG) by stimulation of the perforant path (PP) is known to vary with ongoing behavior and with brain temperature. To further study these phenomena chronic stimulating and recording electrodes were implanted into the PP and DG of rats, and a thermistor was implanted into the contralateral homotopic DG. Field potentials and brain temperature records were made during (1) slow wave sleep (SWS), (2) radiant heating, (3) immersion in cool water, (4) a control session during which no manipulations were made, and (5) under urethane anesthesia. In another group of rats field potentials were recorded during (1) baseline immobile wakefulness, (2) SWS, (3) before SWS or after gentle awakening from SWS (eyes open and presence of intermittent slow waves in the EEG), (4) immobile wakefulness, and (5) 24 h later. Findings were that field EPSP slope decreased and population spike (PS) amplitude increased by up to 60% of baseline values during conditions in which brain temperature was reduced (SWS, immersion in cool water, urethane anesthesia). Conversely, EPSP slope increased and PS amplitude decreased by up to 100% of baseline values during conditions in which brain temperature increased (awakening from SWS, radiant heating, and warming after immersion in cool water or urethane anesthesia). Product moment correlations between brain temperature and field potential measures confirmed the statistical reliability of these findings and accounted for up to 77% of the variance. These findings confirm the robust effect on hippocampal field potentials of brain temperature changes due to exogenous heating and cooling, and extend this effect to anesthetic- and sleep-induced brain temperature changes. They also identify a state that behaviorally resembles quiet wakefulness but resembles SWS in terms of neocortical EEG, brain temperature, and hippocampal field potential measures. The findings indicate the need to control for brain temperature-mediated changes in hippocampal research that uses the dentate gyrus field potential as a dependent measure.

Analysis of Variance↗

PubMed1997

Lactation reduces Fos induction in the paraventricular and supraoptic nuclei of the hypothalamus after urethane administration in rats.

Both neuroendocrine and behavioral responses to stressors are reduced in lactating animals. In these studies we determined whether Fos induction following treatment with urethane would differ between nonlactating and lactating rats. Urethane treatment produced robust Fos expression in the central nucleus of the amygdala and the paraventricular and supraoptic nuclei of the hypothalamus 1 h after treatment. Fos expression in both the paraventricular and supraoptic nuclei was attenuated in lactating rats compared to that seen in nonlactating animals but Fos expression in the central nucleus of the amygdala did not differ between these two groups. Removing litters from lactating rats 48 h prior to urethane administration restored the Fos response in the parvocellular division of the paraventricular nucleus (PVN) to the level seen in nonlactating rats.

Amygdala↗

PubMed1999

Cardiovascular effects of catecholamines injected into the DBB of rats, influence of urethane anaesthesia and local colchicine.

In a previous publication it was shown that 1 microgram colchicine injected into the diagonal band of Broca (DBB) produced a significant decrease in femoral artery blood pressure (and/or volume) measured in urethane-anaesthetised rats. In order to test if the central catecholamines were involved in this effect, guide cannulae were implanted in the DBB and a catheter in the femoral artery. On-line pressure recordings were taken before during and after alpha1, alpha2 and beta adrenoreceptor agonists and antagonists were injected into the region of the DBB of non-anaesthetised and urethane anaesthetised male Wistar rats with and without injection of colchicine. Arterial pressure was significantly increased in the non-anaesthetised rats (114.6+/-2.6 n=11 vs. 149.3+/-3.3 mmHg n=12, p<0.01) yet significantly reduced (82.0+/-3.9 n=11 vs. 63.8+/-4.5 mmHg n=12, p<0.01) in the urethane treated rats by the alpha2 agonist clonidine. The alpha2 antagonist yohimbine blocked these effects in both preparations. In contrast, the beta adrenoreceptor agonist isoprenaline produced a significant decrease in arterial pressure in both preparations (107.7+/-3.9 n=11 vs. 85.9+/-4.0 mmHg n=12, p<0.01) (102.6+/-6.7 n=11 vs. 81.7+/-3.4 mmHg n=12, p<0.01) and this effect was blocked by the beta antagonist propranolol. Colchicine injected into the DBB abolished the effects of the alpha2 agonist and antagonist in the non-anaesthetised but not the anaesthetised rats. The responses to the beta agonist and antagonist were not greatly affected by the colchicine in the non-anaesthetised rats whereas in the anaesthetised rat beta agonist injection tended to totally depress arterial pressure. These results suggest that the sympathetic nervous system in the DBB plays a significant role in the central control of arterial pressure and that the alpha2 component is significantly affected by the state of anaesthesia.

Adrenergic beta-Agonists↗

PubMed1999

Urethane-induced somatostatin mediated inhibition of gastric acid: reversal by the somatostatin 2 receptor antagonist, PRL-2903.

Urethane increases the release of somatostatin (SRIF) which inhibits gastric acid secretion. The SRIF monoclonal antibody, CURE.S6 and the novel sst2 antagonist, PRL-2903 injected intravenously at maximal effective doses increased gastric acid secretion by 2 and 10 fold respectively from basal values within 30 min in urethane-anesthetized rats. Plasma gastrin levels were elevated 2.5 fold within 15 min by PRL-2903 (1.3 micromol/kg, i.v.). These data indicate that the low gastrin and acid secretion levels induced by urethane result from endogenous SRIF acting on sst2 and that PRL-2903 is a valuable SRIF antagonist to assess sst2 mediated events.

Anesthetics, Intravenous↗

PubMed2000

Promotive effect of diethylstilbestrol on urethan-induced mouse lung tumorigenesis.

The effect of diethylstilbestrol (DES) on urethan-induced mouse lung tumorigenesis was assessed by a single intraperitoneal injecting of urethan (50 mg/kg) or/and multi intramuscular injecting of DES (5 or 50 mg/kg). All mice were sacrificed 18 weeks after administration, and the lung tumors were examined histopathologically. DES did not produce an elevated lung tumor response when administered alone, but it produced a statistically significant enhancement of incidence of tumors, average number of tumors, incidence of cancers and constituent ratio of malignant tumors when given in conjunction with urethan. The results indicated that DES may be a promoter in lung tumor formation.

Animals↗

PubMed2001

Urethane anesthesia produces selective damage in the piriform cortex of the developing brain.

The potential induction of neuronal death by neuroactive drugs at specific stages of embryonic or postnatal development is a serious concern in treating brain disease. Recent evidence indicates that NMDA antagonists, GABA agonists, ethanol and some anesthetics can all produce massive neuronal cell loss at critical times during development. We show here that the anesthetic urethane, once used clinically, produces a selective lesion of the piriform cortex, a region not previously implicated in such toxicity, in the developing brain. Young rats were injected with urethane at 1, 2, 3, and 4 weeks of age and brain damage was measured 1-4 days later. We found that urethane produces a large lesion in subfields of the piriform cortex and that the damage is most severe in 2 week-old animals. These data, together with other recent reports, show that there are multiple neuronal death-inducing pathways in the developing nervous system. It will be important to determine if anesthetics used in pregnant women and young children may have similar effects.

Age Factors↗

PubMed2003

Chloral hydrate and ethanol, but not urethane, alter the clearance of exogenous dopamine recorded by chronoamperometry in striatum of unrestrained rats.

Several general anesthetics reduce dopamine (DA) neuronal activity and release. However, anesthetic-induced alterations in DA transporter (DAT) function are unclear. We used high-speed chronoamperometry to examine how urethane, chloral hydrate and ethanol affected clearance of locally-applied DA in the dorsal striatum of unrestrained rats. Maximal DA signal amplitudes (A(max)) and signal decay rate constants (k) were monitored continuously from the awake to anesthetized state. Urethane did not significantly change A(max) or k. Chloral hydrate and ethanol potentiated A(max) by 32% and 37%, respectively, over baseline, indicative of DAT inhibition. These effects were not additive. Only ethanol increased k, an effect blocked by chloral hydrate. These results suggest differential effects of anesthetics on striatal DAT function, with chloral hydrate and ethanol significantly altering DAT activity but urethane producing only minimal effects.

Anesthetics, General↗

PubMed1999

Pontine carbachol elicits multiple rapid eye movement sleep-like neural events in urethane-anaesthetized rats.

Microinjection of a cholinergic agonist, carbachol, into the pontine reticular formation of chronically instrumented intact or acutely decerebrate rats and cats has been used extensively to study rapid eye movement sleep mechanisms. In this study, we sought to develop a reduced carbachol model of rapid eye movement sleep-like neural events exhibiting multiple physiological markers of this state, and allowing for the use of invasive electrophysiological techniques. Accordingly, we investigated whether pontine carbachol could produce rapid eye movement sleep-like motor atonia and electrocortical changes in urethane-anaesthetized rats. We recorded cortical and hippocampal electroencephalograms and genioglossus and inspiratory intercostal muscle activities in 13 urethane-anaesthetized, spontaneously breathing, tracheotomized and vagotomized rats. In steady-state periods with high-voltage/low-frequency electroencephalogram activity, carbachol microinjections (15-40 nl, 10 mM) were placed in the medial pontine reticular formation. In 12 rats, carbachol elicited episodes of stereotyped hypotonia of genioglossus but not intercostal muscle activity, typical of rapid eye movement sleep, with a latency and duration of 2.2+/-0.3min (mean+/-S.E.M.) and 11.0+/-2.9 min, respectively. In four of these rats, also similar to rapid eye movement sleep, the major suppression of genioglossus activity (-74+/-9%) was accompanied by electroencephalogram desynchronization, appearance of hippocampal theta rhythm, and a respiratory rate increase (+ 14+/-3%). In the remaining eight rats, the stereotyped suppression of genioglossus activity (-48+/-3%) occurred without electroencephalogram desynchronization and hippocampal theta, and was accompanied by a respiratory rate decrease (-6+/-2%); a pattern of response typical of decerebrate animals. Within a rat, similar patterns of response to repeated carbachol injections at the same anatomical site were obtained. Pontine atropine prevented responses to subsequent carbachol injections. Thus, in urethane-anaesthetized rats, pontine carbachol consistently produced a differential suppression of pharyngeal versus respiratory pump muscle activity, and in a subset of animals, this was also accompanied by cortical and hippocampal electrographic changes typical of rapid eye movement sleep. This shows that complex and stereotyped neuronal events underlying both ascending and descending signs of rapid eye movement sleep can be pharmacologically activated under general anaesthesia. Such a reduced preparation may be useful for studies into the central neuronal mechanisms underlying generation of rapid eye movement sleep; particularly for studies requiring techniques that are difficult to implement in intact, naturally sleeping animals. The acceleration of the respiratory rate observed only when carbachol induced electroencephalogram desynchronization suggests that neural events associated with electrocortical changes contribute to the respiratory rate increases observed in natural rapid eye movement sleep.

Anesthesia↗

PubMed1997

Relations between acetylcholine release and electrophysiological characteristics of theta rhythm: a microdialysis study in the urethane-anesthetized rat hippocampus.

In urethane-anesthetized rats, recording electrodes were implanted in the left dorsal hippocampus and a dialysis probe was placed in the contralateral dorsal or ventral hippocampus. Samples of extracellular acetylcholine (ACh) levels were assessed at 10-min intervals over a period of 30 min using microdialysis with high-performance liquid chromatography with electrochemical detection. EEG was recorded during the same period and amplitude, frequency, and duration of theta rhythm were calculated for each of the three 10-min intervals. Data were analyzed using the two-tailed Spearman rank-order correlation test. A positive and high rank correlation coefficient (rho = 0.90, p < 0.01, n = 8) was seen between the average ACh outflow in the dorsal hippocampus and the average theta amplitude, both being calculated for the entire collection period. A lower but statistically significant positive correlation (rho = 0.59, p < 0.01) between dorsal hippocampus ACh output and theta amplitude was also found when the couples of values collected for the 30-min period were pooled (n = 20). In contrast, frequency and duration of theta were not significantly correlated with dorsal hippocampus ACh release. Also, no statistically significant correlation (p > 0.05) was found between ACh output in the ventral hippocampus and theta parameters. Because changes in hippocampal ACh outflow are believed to be the reflection of changes in number and/or level of activity of cholinergic afferents to the dorsal hippocampus, our present findings support the view that, at least in the dorsal hippocampus of the urethane-anesthetized rat, the septohippocampal cholinergic projection regulates the theta amplitude but not frequency. Finally, the possibility that ACh outflow increase and tonic release in the hippocampus is not a sufficient condition to induce and maintain theta in the urethane-anesthetized rat is discussed.

Acetylcholine↗

PubMed2002

Metabolism of carcinogenic urethane to nitric oxide is involved in oxidative DNA damage.

Carcinogenic urethane (ethyl carbamate) forms DNA adduct via epoxide, whereas carcinogenic methyl carbamate can not. To clarify a mechanism independent of DNA adduct formation, we examined DNA damage induced by N-hydroxyurethane, a urethane metabolite, using 32P-5'-end-labeled DNA fragments. N-hydroxyurethane induced Cu(II)-mediated DNA damage especially at thymine and cytosine residues. DNA damage was inhibited by both catalase and bathocuproine, suggesting a role for H(2)O(2) and Cu(I) in DNA damage. Free (*) OH scavengers did not inhibit the DNA damage, although methional did inhibit it. These results suggest that reactive species, such as the Cu(I)-hydroperoxo complex, cause DNA damage. Formation of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) was increased by N-hydroxyurethane in the presence of Cu(II). When treated with esterase, N-hydroxyurethane induced 8-oxodG formation to a similar extent as that induced by hydroxylamine. Enhancement of DNA cleavages by endonuclease IV suggests that hydroxylamine induced depurination. Furthermore, hydroxylamine induced a significant increase in 8-oxodG formation in HL-60 cells but not in its H(2)O(2)-resistant clone HP 100 cells. o-Phenanthroline significantly inhibited the 8-oxodG formation in HL-60 cells, confirming the involvement of metal ions in the 8-oxodG formation by hydroxylamine. Electron spin resonance spectroscopy, utilizing Fe[N-(dithiocarboxy)sarcosine](3), demonstrated that nitric oxide (NO) was generated from hydroxylamine and esterase-treated N-hydroxyurethane. It is concluded that urethane may induce carcinogenesis through oxidation and, to a lesser extent, depurination of DNA by its metabolites.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed1975

Cell kinetics of urethane induced murine pulmonary adenomata: I. The growth rate.

A single injection of urethane into adult male A2G mice produced an increase in the proliferative rate of alveolar wall cells, reaching a peak at 2 weeks post urethan (PU) and declining to control levels by 2 months PU. During this urethane induced proliferative response the single and double labelling indices and the native metaphase index were all elevated although there was no corresponding alteration in the arrested metaphase index. This proliferative response may not be restricted to hyperplasia of potentially neoplastic cells, such as type II epithelium, but may also include type I epithelial cells and alveolar macrophage precursors. However, it was impossible to identify individual cell populations by methods used. The growth rate of adenomata decrease with time and cell kinetic techniques showed that the rates of entry of adenoma cells into DNA synthesis and into metaphase were decreasing concurrently with the growth rate. Thus the rate of cell production falls as adenomata age but how much cell loss contributes to the decrease in growth rate is not yet known. Decreasing cell production could be due to an increased cell cycle time and/or a decreased growth fraction. The duration of DNA synthesis in adenomata increased markedly as the mice survived, suggesting that the cell cycle time might be increased, but further experiments are required to determine whether the growth fraction changes. Attention is drawn to a complication that Colcemid introduces into kinetic studies on alveolar wall cells.

Adenoma↗

PubMed1978

Renal vascular response to haemorrhage in the rabbit after pentobarbitone, chloralose-urethane and ether anaesthesia.

1. Total renal blood flow and its cortical distribution were measured by the microsphere technique before and after haemorrhage in conscious rabbits, and after haemorrhage in rabbits anaesthetized with pentobarbitone, chloralose-urethane or ether. 2. The average blood loss necessary to achieve a fall in systolic blood pressure to about 65 mmHg was 101 ml in conscious rabbits and 38, 90 and 118 ml in weight-matched groups of rabbits anaesthetized with pentobarbitone, chloralose-urethane and ether respectively. 3. After haemorrhage in conscious rabbits total renal blood flow fell by 25%, this fall being confined to the superficial renal cortex. 4. In rabbits subject to haemorrhage under pentobarbitone anaesthesia renal blood flow fell by a further 23% when compared with the conscious bled rabbits. This reduction in blood flow was confined to the superficial cortex. 5. Haemorrhage in the rabbits subjected to chloralose-urethane anaesthesia caused no significant change in renal blood flow, as compared with conscious bled rabbits. 6. Haemorrhage under ether anaesthesia was associated with a further 33% fall in total renal blood flow, as compared with conscious bled rabbits. This was associated with a fall of 32% and 34% in superficial and deep cortical blood flow respectively. 7. Animals subjected to general anaesthesia may be particularly susceptible to the renal haemodynamic effects of haemorrhage.

Anesthesia, General↗

PubMed2001

Effect of nitric oxide synthase inhibition on fos expression in the hypothalamus of female rats following central oxytocin and systemic urethane administration.

Three experiments were carried out to investigate the pattern of neuronal activation induced by central oxytocin administration and its modulation by nitric oxide (NO). First, we compared the induction of Fos-like immunoreactivity (lir) in the supraoptic (SON) and paraventricular (PVN) nuclei and medial preoptic area (MPOA) after central oxytocin administration between nonlactating and lactating rats. Next, we investigated whether NO modulated Fos induction following central oxytocin administration using a nitric oxide synthase (NOS) inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME). Finally, to determine whether the effects of NOS inhibition on Fos induction would generalize to stimuli other than oxytocin, we compared Fos-lir in the SON and PVN of lactating and nonlactating rats following L-NAME and urethane administration. In the first two experiments, oxytocin (50 ng in 2 microl) or vehicle was administered into the third ventricle. L-NAME (50 mg/kg) was given by an intraperitoneal (i.p.) injection 30 min before oxytocin administration (experiment 2) or an i.p. injection of urethane (1.4 g/kg) (experiment 3). In all experiments, lactating rats were tested on day 12 or 13 postpartum and nonlactating females at least 11 days after surgery or the start of the experiment. Central oxytocin infusion induced Fos expression in the SON and PVN in lactating and nonlactating rats and in the MPOA and bed nucleus of the stria terminalis in lactating rats. Overall, lactating rats that received L-NAME and oxytocin had a greater number of cells showing Fos-lir in both the SON and PVN. Conversely, L-NAME administration reduced Fos-lir in the SON and PVN in oxytocin-stimulated nonlactating rats. In urethane-treated rats, L-NAME administration did not change Fos-lir in lactating rats but reduced Fos-lir in nonlactating rats. These data suggest that the role of NO in modulating the activity of neurones in discrete nuclei in the hypothalamus varies across reproductive state and with the stimulus presented.

Animals↗

PubMed1987

Antiteratogenic and anticarcinogenic effects of X-rays in urethane-treated NMRI mice.

A single intraperitoneal injection of urethane (ethyl carbamate) induces lung tumours in 80 per cent of male and 100 per cent of female NMRI mice, respectively. In the course of time the initially benign adenomatous tumours can develop into malignant adenomatosis of the lung (alveolar cell carcinoma). For an analysis of the mechanisms of tumour development and the possible interactions involved, low doses of X-rays (5-100 cGy) were administered 6 hours after urethane treatment. A significant anticarcinogenic and, also, anti-teratogenic action was observed. This implies that in both cases similar mechanisms are involved. Single injections of vitamin C or chloroquine counteract the urethane effects in the same manner as do the low doses of X-rays, but probably by different mechanisms.

Abnormalities, Drug-Induced↗