potassium-bromate and Body-Weight

Potassium bromate (KBrO3) has been reported to be toxic, adversely affecting many body tissues and organs. The aim of this study was to determine the blood coagulation effect of Parkia biglobosa (P. biglobosa) seed on potassium bromate induced coagulopathy.. P. biglobosa was extracted with soxhlet extractor with ethanol as the solvent. Twenty-four adult male Wistar rats were acclimatized under laboratory conditions and were randomly grouped into A, B, C and D. Group A was given distilled water orally. Animals in groups B, C and D were administered 100 mg/kg body weight of potassium bromate, but groups C and D were also treated with 100 and 200 mg/kg body weight of P. biglobosa respectively. Both potassium bromate and P. biglobosa were freshly prepared on daily basis and administered to rats by oral gavage for 28 days. At the end of the treatment period, blood samples were collected in sodium citrate bottles and were used for analysis of Prothrombin Time (PT), Activated Partial Thromboplastin Time (APTT), Thrombin Time (TT), fibrinogen and vitamin K levels using standard methods.. Administration of potassium bromate increased Prothrombin Time (PT) from 11.67±2.15 seconds (in control animals) to 19.53±2.83 seconds. Treatment with 100 and 200 mg/kg body weight of P. biglobosa seed extract neutralized this effect in a dose-dependent manner. Likewise, KBrO 3 was observed to have significantly elevated Activated Partial Thromboplastin Time (APTT) from 29.67±3.93 to 41.10±4.79 seconds and Thrombin Time (TT) from 15.36±2.06 to 25.43±2.83 seconds when compared with those in the control group. The result further showed that exposure of animals to KBrO3 significantly declined the levels of fibrinogen (from 4.05±0.72 to 2.59±0.30 g/dL) and vitamin K (from 3.18±0.73 to 1.84±0.18 ng/mL) when compared with the untreated animals. The effect of KBrO 3 on PT, APTT, TT, Fibrinogen and vitamin k were attenuated by P. biglobosa in a dose-dependent manner.. The results of this investigation demonstrated that potassium bromate caused prolongation of PT, aPTT and TT and decreased levels of fibrinogen and vitamin K, but P. biglobosa treatment counteracted these effects. Thus, it is recommended that these results be investigated in clinical trials in human volunteers.. On a signalé que le bromate de potassium (KBrO3) est toxique et qu’il a des effets néfastes sur de nombreux tissus et organes du corps. Le but de cette étude était de déterminer l’effet de la graine de Parkia biglobosa (P. biglobosa) sur la coagulopathie induite par le bromate de potassium.. P. biglobosa a été extrait à l’aide d’un extracteur soxhlet avec de l’éthanol comme solvant. Vingt-quatre rats Wistar mâles adultes ont été acclimatés dans des conditions de laboratoire et ont été répartis au hasard en groupes A, B, C et D. Le groupe A a reçu de l’eau distillée par voie orale. Les animaux des groupes B, C et D ont reçu 100 mg/kg de poids corporel de bromate de potassium, mais les groupes C et D ont également été traités avec 100 et 200 mg/kg de poids corporel de P. biglobosa respectivement. Le bromate de potassium et P. biglobosa ont été fraîchement préparés quotidiennement et administrés aux rats par gavage oral pendant 28 jours. A la fin de la période de traitement, des échantillons de sang ont été collectés dans des bouteilles de citrate de sodium et ont été utilisés pour l’analyse du temps de prothrombine (PT), du temps de thromboplastine partielle activée (APTT), du temps de thrombine (TT), du fibrinogène et des niveaux de vitamine K en utilisant des méthodes standard.. L’administration de bromate de potassium a augmenté le temps de prothrombine (PT) de 11,67±2,15 secondes (chez les animaux témoins) à 19,53±2,83 secondes. Un traitement avec 100 et 200 mg/kg de poids corporel a neutralisé cet effet de manière dose-dépendante. De même, on a observé que le KBrO3 augmentait significativement le temps de thromboplastine partielle activée (TCA) de 29,67±3,93 à 41,10±4,79 secondes et le temps de thrombine (TT) de 15,36±2,06 à 25,43±2,83 secondes par rapport aux animaux du groupe témoin. Le résultat a également montré que l’exposition des animaux au KBrO3 a réduit de manière significative les niveaux de fibrinogène (de 4,05±0,72 à 2,59±0,30 g/dL) et de vitamine K (de 3,18±0,73 à 1,84±0,18 ng/mL) par rapport aux animaux non traités. L’effet du KBrO3 sur le PT, l’aPTT, le TT, le Fibrinogène et la vitamine K a été atténué par P. biglobosa de manière dose-dépendante.. Les résultats de cette étude ont démontré que le bromate de potassium a provoqué une prolongation du PT, de l’aPTT et du TT et a diminué les niveaux de fibrinogène et de vitamine K, mais le traitement par P. biglobosa a contrecarré cet effet. Il est donc recommandé que ces résultats soient étudiés dans des essais cliniques sur des volontaires humains.. Coagulation sanguine, Coagulopathie, Parkia biglobosa, Bromate de potassium.

Topics: Adult; Animals; Blood Coagulation; Body Weight; Fibrinogen; Humans; Male; Rats; Rats, Wistar; Vitamin K

Potassium bromate (KBrO3) is widely used as a food additive and is a major water disinfection by-product. The present study reports the side effects of KBrO3 administration on the brain functions and behaviour of albino mice.. Animals were divided into three groups: control, low dose KBrO3 (100 mg/kg/day) and high dose KBrO3 (200 mg/kg/day) groups.. Administration of KBrO3 led to a significant change in the body weight in the animals of the high dose group in the first, second and the last weeks while water consumption was not significantly changed. Neurobehavioral changes and a reduced Neurotransmitters levels were observed in both KBrO3 groups of mice. Also, the brain level of reduced glutathione (GSH) in KBrO3 receiving animals was decreased. Histological studies favoured these biochemical results showing extensive damage in the histological sections of brain of KBrO3-treated animals.. These results show that KBrO3 has serious damaging effects on the central nervous system and therefore, its use should be avoided.

Topics: Administration, Oral; Animals; Body Weight; Brain; Bromates; Dose-Response Relationship, Drug; Food Additives; Glutathione; Male; Mice; Neurotransmitter Agents; Oxidative Stress

The food additive potassium bromate (KBrO3) is known as a renal carcinogen and causes chromosomal aberrations in vitro without metabolic activation and in vivo in hematopoietic and renal cells. As a part of a collaborative study by the Mammalian Mutagenicity Study group, which is a subgroup of the Japanese Environmental Mutagen Society, we administered KBrO3 to rats orally for 4, 14, and 28 days and examined the micronucleated (MNed) cell frequency in the liver, glandular stomach, colon, and bone marrow to confirm whether the genotoxic carcinogen targeting other than liver and gastrointestinal (GI) tract was detected by the repeated dose liver and GI tract micronucleus (MN) assays. In our study, animals treated with KBrO3 showed some signs of toxicity in the kidney and/or stomach. KBrO3 did not increase the frequency of MNed cells in the liver and colon in any of the repeated dose studies. However, KBrO3 increased the frequency of MNed cells in the glandular stomach and bone marrow. Additionally, the MNed cell frequency in the glandular stomach was not significantly affected by the difference in the length of the administration period. These results suggest that performing the MN assay using the glandular stomach, which is the first tissue to contact agents after oral ingestion, is useful for evaluating the genotoxic potential of chemicals and that the glandular stomach MN assay could be integrated into general toxicity studies.

Topics: Administration, Oral; Age Factors; Animals; Body Weight; Bone Marrow; Bromates; Carcinogens; Chromosome Aberrations; Colon; Cooperative Behavior; Dose-Response Relationship, Drug; Drug Administration Schedule; Hepatocytes; Humans; Japan; Kidney; Liver; Male; Micronucleus Tests; Organ Specificity; Rats; Rats, Sprague-Dawley; Societies, Pharmaceutical; Stomach

Bromate is a byproduct of water disinfection that is produced when waters contain bromide treated with ozone. To investigate the level of the toxicity of bromate and find the most sensitive indicators in a short time, a series of toxicological assessments were conducted including the acute toxicity, cumulative toxicity, genetic toxicity and subacute toxicity of bromate (using Potassium Bromate to represent bromate). The LD50 of orally administered Potassium Bromate was 215 mg/kg in Wistar rats and 464 mg/kg in ICR mice. The cumulative toxicity of Potassium Bromate was not obvious. The Ames test, mouse bone marrow cell micronucleus test and mouse sperm abnormality test did not indicate mutagenicity. The results of the subacute study did not exhibit significant differences in most of the parameters, except the white blood cell count, which was significantly decreased in male rats. In addition, Potassium Bromate influenced the albumin, creatinine, total cholesterol, triglycerides and glucose levels in male rats to various extents. A thorough analysis of the above tests clearly demonstrates that bromate has toxicity, not obvious cumulative toxicity and the white blood cell count can be used as an indicator to reflect the toxicity of bromate and investigate bromate's toxic mechanism.

Topics: Administration, Oral; Animals; Biomarkers; Body Weight; Bromates; Dose-Response Relationship, Drug; Drinking; Eating; Female; Lethal Dose 50; Leukocytes; Male; Mice, Inbred ICR; Micronucleus Tests; Rats, Wistar; Risk Assessment; Spermatozoa; Time Factors; Toxicity Tests, Acute; Water Pollutants, Chemical; Water Purification

Male F344 rats were exposed to potassium bromate (KBrO₃) in drinking water at concentrations of 0, 5, 20, 100, 200, or 400 mg/L for 2 or 13 weeks. Endpoints evaluated included clinical observations, body weights, serum chemistry, gross pathology, organ weights, and select tissue histopathology (kidney, lung, liver, thyroid, and tunica vaginalis). Weekly body weight and water consumption means were similar between KBrO₃ and control groups throughout the study. Increases in kidney weights were observed in rats of the 400 mg/L group following 2- or 13-weeks exposure. Hyaline droplets were observed in renal tubules of rats of the 200 and 400 mg/L groups following 2 weeks exposure and in rats of the 400 mg/L group at 13 weeks. There were no KBrO₃-related microscopic findings in the lung, liver, thyroid, and tunica vaginalis at the 2- and 13-week time points. A no observed effect level of 100 mg/L KBrO₃ (8.1 mg/kg/day) was selected based on the absence of microscopic alterations in the kidney.

Topics: Animals; Blood Chemical Analysis; Body Weight; Bromates; Drinking; Endpoint Determination; Kidney; Kidney Diseases; Liver; Male; No-Observed-Adverse-Effect Level; Organ Size; Rats; Rats, Inbred F344; Thyroid Gland

As susceptibility to carcinogens varies considerably among different strains of experimental animals, evaluation of dose-response relationships for genotoxic carcinogen in different strains is indispensable for risk assessment. Potassium bromate (KBrO(3)) is a genotoxic carcinogen inducing kidney cancers at high doses in male F344 rats, but little is known about its carcinogenic effects in other strains of rats. The purpose of the present study was to determine dose-response relationships for carcinogenic effects of KBrO(3) on N-ethyl-N-hydroxyethylnitrosamine (EHEN)-induced kidney carcinogenesis in male Wistar rats. We found that KBrO(3) showed significant enhancement effects on EHEN-induced kidney carcinogenesis at above 250 ppm but not at doses of 125 ppm and below when evaluated in terms of induction of either preneoplastic lesions or tumors in male Wistar rats. Furthermore, KBrO(3) significantly increased the formation of oxidative DNA damage at doses of 125 and above but not at doses of 30 ppm and below in kidneys. These results demonstrated that low doses of KBrO(3) exert no effects on development of EHEN-initiated kidney lesions and induction of oxidative DNA damage. Taking account of previous similar findings in male F344 rats, it is strongly suggested that a threshold dose exists for enhancement effects of KBrO(3) on kidney carcinogenesis in rats.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Animals; Body Weight; Bromates; Carcinogens; Deoxyguanosine; Diethylnitrosamine; DNA Damage; DNA Repair; Dose-Response Relationship, Drug; Gene Expression; Kidney; Kidney Neoplasms; Male; Organ Size; Oxidative Stress; Rats; Rats, Wistar; RNA, Messenger

Potassium bromate (KBrO3) has been classified as a genotoxic carcinogen based on positive results in the Ames test, and chromosome aberration and micronucleus tests. The purpose of the present study was to investigate the dose-response relationship for in vivo mutagenic and toxic effects of KBrO3 in the kidneys of Big Blue rats. In experiment 1, male Big Blue rats were divided into 8 groups. KBrO3 was dissolved in tap water and administered to groups 1-8 at concentrations of 0, 0.02, 0.2, 2, 8, 30, 125 and 500 ppm, respectively, for 16 weeks. Experiment 2 was performed to investigate the effects of KBrO3 at the 0.002 ppm dose approximately contained in the tap water on rat kidneys. Ten Big Blue rats were divided into 2 groups and given distilled water and tap water, respectively, for 16 weeks. In experiment 1, treatment with 500 ppm KBrO3 significantly increased the mutant and total mutation frequencies and frequency of GC to TA transversion of the lacI gene in the kidney compared to non-treatment control group, but 125 ppm and lower doses of KBrO3 had no effects. Histopathologically, renal toxic changes were observed in groups administered KBrO3 at 30 ppm or higher in a dose-dependent manner. PCNA positive cell indices in renal tubular cells were significantly increased in the kidney at doses of 125 and 500 ppm, but not at 30 ppm or lower doses, as compared to the control group. Furthermore, 8-hydroxy-2'-deoxyguanosine formation, a marker of oxidative stress, was significantly increased at 500 ppm. In experiment 2, there were no differences in any parameter between the distilled water and tap water groups. These results suggest the existence of no-effect levels for in vivo mutagenic and toxic effects, proliferation stimulus, and oxidative stress of KBrO3 in rat kidneys.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Animals; Body Weight; Bromates; Cell Proliferation; Deoxyguanosine; DNA; Dose-Response Relationship, Drug; Drug Evaluation, Preclinical; Kidney; Male; Mutagenicity Tests; Mutation; Organ Size; Proliferating Cell Nuclear Antigen; Rats; Rats, Inbred F344; Rats, Mutant Strains

Disinfection of drinking water has been one of the greatest public health successes. Numerous halogenated disinfection by-products (DBPs) occur and chronic ingestion has been associated with an increased risk for colorectal cancer in human populations. Because the intestinal microbiota can bioactivate xenobiotics, studies have been performed to examine the effects of individual DBPs on intestinal microbial metabolism. No studies have been conducted on a defined mixture of DBPs to determine if there is an enhancement of response to a mixture. Ten-week-old male Long-Evans rats were treated in their drinking water for 17 weeks with 0.4 g/l potassium bromate, 1.8 g/l chloroform, 0.7 g/l bromodichloromethane (BDCM), 0.07 g/l 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX), or a mixture of the four chemicals or distilled water. Cecal nitroreductase (NR), azoreductase (AR), dechlorinase (DC), beta-glucuronidase (GLR), beta-galactosidase (GAL), and beta-glucosidase (GLU) were assayed. No change in GLU or GLR activity was detected after treatment. BDCM treatment reduced DC and GAL activities and elevated NR and AR activity. GAL, AR, and NR activities were significantly different after treatment with bromate, chloroform, BDCM, and MX, but not the mixture. DC activity after chloroform-, MX-, or BDCM-treatment was significantly below control levels. The present study shows that changes in intestinal microbial metabolism do occur after treatment with individual and a mixture of DBPs but the changes were not additive in the mixture group.

Topics: Animals; Bacteria; beta-Galactosidase; beta-Glucosidase; Body Weight; Bromates; Cecum; Chloroform; Drug Combinations; Furans; Glucuronidase; Heterozygote; Male; Mutagens; NADH, NADPH Oxidoreductases; Nitroreductases; Rats; Rats, Long-Evans; Repressor Proteins; Trihalomethanes; Tuberous Sclerosis Complex 2 Protein; Tumor Suppressor Proteins; Water Pollutants, Chemical

Potassium bromate (KBrO3) is a potent nephrotoxic agent. In this paper, we report the chemopreventive effect of Nigella sativa (black cumin) on KBrO3-mediated renal oxidative stress, toxicity and tumor promotion response in rats. KBrO3 (125 mg/kg body weight, intraperitoneally) enhances lipid peroxidation, gamma-glutamyl transpeptidase, hydrogen peroxide and xanthine oxidase with reduction in the activities of renal antioxidant enzymes and renal glutathione content. A marked increase in blood urea nitrogen and serum creatinine has also been observed. KBrO3 treatment also enhances ornithine decarboxylase (ODC) activity and [3H] thymidine incorporation into renal DNA. Prophylaxis of rats orally with Nigella sativa extract (50 mg/kg body weight and 100 mg/kg body weight) resulted in a significant decrease in renal microsomal lipid peroxidation (P < 0.001), gamma-glutamyl transpeptidase (P < 0.001), H2O2 (P < 0.001) and xanthine oxidase (P < 0.05). There was significant recovery of renal glutathione content (P < 0.01) and antioxidant enzymes (P < 0.001). There was also reversal in the enhancement of blood urea nitrogen, serum creatinine, renal ODC activity and DNA synthesis (P < 0.001). Data suggest that Nigella sativa is a potent chemopreventive agent and may suppress KBrO3-mediated renal oxidative stress, toxicity and tumour promotion response in rats.

Topics: Animals; Antidotes; Blood Urea Nitrogen; Body Weight; Bromates; Carcinogens; Female; gamma-Glutamyltransferase; Glutathione; Kidney; Lipid Peroxidation; Microsomes; Nigella sativa; Oxidative Stress; Phytotherapy; Plant Extracts; Rats

Potassium bromate (KBrO3) is known to be an oxidizing agent that is used not only as a food additive, mainly in the bread-making process, but also as a neutralizer in thioglycolate containing hair curling set. Although it has been shown that bromate poisoning could cause severe and irreversible sensorineural hearing loss as well as renal failure, the action mechanism of bromate-induced otoneurotoxicity especially its combination with thioglycolate remains to be studied. In this study, we attempted to investigate the toxic effects of KBrO3 in combination with or without thioglycolate on the auditory brainstem response (ABR) system in the guinea-pigs which was claimed to be very susceptible to the xenobiotics. In a preliminary test, we have found that after consecutive 2 weeks administration, KBrO3 caused a significant prolongation of wave I-III and the interwave latencies of ABR as well as significantly elevated the threshold of hearing, suggesting that the conduction velocity of the peripheral auditory nerve was delayed. By contrast, the absolute latency of wave IV/V and the interwave latency of wave III-V were not significantly prolonged, suggesting that KBrO3 had no effect on the brainstem. This oto-neurotoxic effect of KBrO3 was markedly enhanced by combining with thioglycolate. Our data also indicated that KBrO3 combined with thioglycolate but not KBrO3 alone prominantly caused a decrease of body weight. However, enzymatic activities (including Na+/K+-ATPase and Ca2+-ATPase) and the level of nitric oxide (NO) was significantly affected in the brainstem. Based on these findings, we tentatively conclude that whether KBrO3 alone or KBrO3 combined with thioglycolate induced oto-neurotoxicity majorly through the peripheral auditory nerve rather than via the central brainstem intoxication.

Topics: Animals; Auditory Threshold; Body Weight; Bromates; Calcium-Transporting ATPases; Cochlear Nerve; Enzyme Activation; Evoked Potentials, Auditory, Brain Stem; Food Additives; Guinea Pigs; Nitric Oxide; Reaction Time; Sodium-Potassium-Exchanging ATPase; Thioglycolates

Free radical scavengers can protect against the genotoxicity induced by chemical carcinogens by decreasing oxidative damage. The protective effect of the antioxidants melatonin, resveratrol, vitamin E, butylated hydroxytoluene and 2-mercaptoethylamine, and the spin-trapping compound alpha-phenyl-N-tert-butyl nitrone (PBN) against oxidative DNA damage was studied in the kidney of rats treated with the kidney-specific carcinogen potassium bromate (KBrO3). KBrO3 was given to rats previously treated with melatonin, resveratrol, PBN, vitamin E, butylated hydroxytoluene, or 2-mercaptoethylamine. Oxidative damage to kidney DNA was estimated 6 hours afterwards by measuring 8-oxo-7,8-dihydro-2'-deoxyguanosine (oxo8dG) referred to deoxyguanosine (dG) by means of high performance liquid chromatography with electrochemical-coulometric and ultraviolet detection. Levels of oxo8dG in the renal genomic DNA significantly increased by more than 100% after the KBrO3 treatment. This increase was completely abolished by the treatment with resveratrol and was partially prevented by melatonin, PBN and vitamin E. Resveratrol and PBN also prevented the increase in relative kidney weight induced by KBrO3. These results show that various different antioxidants and a free radical trap, working in either the water-soluble or the lipid-soluble compartments, can prevent the oxidative DNA damage induced in the kidney by the carcinogen KBrO3.

Topics: Animals; Anticarcinogenic Agents; Antioxidants; Body Weight; Bromates; Carcinogens; Cyclic N-Oxides; DNA Damage; Kidney; Male; Melatonin; Nitrogen Oxides; Organ Size; Rats; Rats, Wistar; Resveratrol; Spin Labels; Stilbenes; Vitamin E

The renal tumour-initiating activity of potassium bromate (KBrO3), a known genotoxic rat renal carcinogen, was investigated in male F344/NCr rats. 6-wk-old rats were given KBrO3 intragastrically as a single dose of 300 mg/kg body weight, which was confirmed by our preliminary toxicity study as a maximum tolerated single dose for this strain of rat. Starting 2 wk after KBrO3 treatment, groups of 39 rats received either a basal diet or a diet containing 4000 ppm barbital sodium (BBNa) as a promoting regimen and were killed at 30, 52, or 104 wk. Control rats received either dietary BBNa (4000 ppm) or the basal diet alone from wk 2 to 52 or 104 wk. Nephropathy was observed in all rats treated with KBrO3 followed by BBNa at 30 wk and in rats receiving BBNa alone, but not in rats exposed to KBrO3 alone. Dysplastic renal tubular cell foci (DTF), putative preneoplastic renal tubular cell lesions were found associated with nephropathy in rats exposed to KBrO3 followed by BBNa from 47 wk. The incidences and multiplicities of DTF and renal tubular cell tumours observed from 31 to 104 wk revealed no initiating effect of KBrO3 treatment. These results indicate that the KBrO3 dose of 300 mg/kg did not initiate renal carcinogenesis.

Topics: Animals; Barbital; Body Weight; Bromates; Carcinogens; Kidney Neoplasms; Male; Organ Size; Rats; Rats, Inbred F344

In order to ascertain the minimum induction time, minimum treatment period and total dose required for development of renal cell tumors, KBrO3 at a concentration of 500 ppm was administered in the drinking water to a total of 232 male F344 rats divided into 14 experimental groups and the development of tumors was examined by two different approaches. In a continued-treatment study, administration of KBrO3 was stopped at week 13, 26, 39, 52 or 104 and rats were immediately sacrificed for comparison with controls given distilled water (DW) alone. Renal cell adenomas were found as early as after 26 weeks of treatment with KBrO3. The yields of dysplastic foci, adenomas and adenocarcinomas of the kidney, follicular cell tumors of the thyroid and mesotheliomas of the peritoneum increased with treatment, the final incidences all being statistically significant after administration of KBrO3 for 104 weeks. To examine the effect of discontinued treatment, on the other hand, the rats were given KBrO3 for the first 13, 26, 39 or 52 weeks and were subsequently maintained on DW alone until sacrifice at week 104. The incidences of tumors in these groups were compared with that of a group continuously administered KBrO3 for 104 weeks. The yields of renal dysplastic foci, adenomas and adenocarcinomas in all discontinued-treatment groups were approximately equal to or even higher than those in the group given KBrO3 continuously for 104 weeks. It is concluded that, under the conditions of this study: the minimum induction time for the development of renal adenomas was 26 weeks and the minimum treatment period and total dose for the induction of renal adenomas and adenocarcinomas were 13 weeks and 4 g/kg, respectively, when the rats were maintained thereafter on DW for 2 years.

Topics: Animals; Body Weight; Bromates; Bromine; Carcinogens; Dose-Response Relationship, Drug; Drinking Behavior; Drug Administration Schedule; Kidney Neoplasms; Male; Rats; Rats, Inbred F344; Thyroid Neoplasms

The carcinogenicity of potassium bromate, a food additive and a neutralizer in permanent waving, was tested by adding it to the drinking water of F344 rats for 110 weeks. Groups of 53 males and 53 females, each, were given solutions of 500 or 250 ppm of potassium bromate or distilled water. A concentration of 500 ppm markedly inhibited an increase of body weight of male rats. The mean survival time was shortest for males given 500 ppm (88.1 +/- 18.1 wk); the survival times of other groups were 101-104 weeks. The percentage survival in week 104 was relatively high in all groups, and it was 77.4% for males and 66.0% for females in the control group. High incidences of renal cell tumors (in males and females given 500 or 250 ppm) and mesotheliomas of the peritoneum (in males given 500 ppm) were observed. The incidences of these tumors in test groups were significantly higher than those in controls (P less than .001). It was concluded that, when orally administered under the conditions of this experiment, potassium bromate was carcinogenic to F344 rats.

Topics: Adenocarcinoma; Adenoma; Animals; Body Weight; Bromates; Bromine; Female; Food Additives; Hair Preparations; Kidney Neoplasms; Male; Mesothelioma; Peritoneal Neoplasms; Probability; Rats; Rats, Inbred F344

Topics: Adipose Tissue; Animals; Body Weight; Bread; Bromates; Bromine; Carcinogens; Eating; Female; Food Additives; Kidney Function Tests; Male; Potassium; Rats; Time Factors