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Biomedical subjects

J R Cabral

Publications and source records attributed to J R Cabral.

At least 37 records · Page 2Linked to original sources
PubMed1986

Influence of ethyl alcohol on the carcinogenic activity of N-nitrosonornicotine.

The present paper describes an experiment designed to investigate the effects of the combined action of different doses of N-nitrosonornicotine (NNN) and ethyl alcohol in BDVI rats. Dose-response relationships of NNN was clearly shown. Ethyl alcohol did not appear to increase, to a great degree, the tumour incidence of NNN. However, ethyl alcohol did shorten the tumour latency period in the groups given NNN in alcoholic solution. In addition, an infiltration of the olfactory tumours to the brain was observed more frequently in both males and females given the high dose of NNN in alcoholic solution.

Animals↗
PubMed1986

Dengue 3 virus transmission in Africa.

The first known transmission of dengue 3 virus in Africa was documented by virus isolation during an epidemic of dengue-like illness in Pemba, Mozambique, in late 1984 and early 1985. Dengue 3 virus was the only serotype isolated. Most patients appeared to be experiencing secondary flavivirus infections, but whether this was the result of previous dengue, yellow fever, or other flavivirus infection is not known. Two cases of hemorrhagic disease with shock and death were associated with the epidemic.

Adolescent↗
PubMed1986

Carcinogenic activity of hexachlorobenzene in mice and hamsters.

Hexachlorobenzene (HCB) has been used as a fungicide, is a contaminant of various pesticides and is a by-product in the manufacture of many other chlorinated hydrocarbons. In Turkey, HCB caused an epidemic of toxic porphyria involving several thousand people between 1955 and 1959. The aim of the present studies was to determine the chronic toxicity of HCB after prolonged oral administration and we report here that HCB is carcinogenic in mice and hamsters. Mice and hamsters were given dietary HCB at doses of 50, 100 and 200 ppm for life, with deaths due to toxic manifestations of HCB occurring in group HCB 200. All survivors were killed after 120 weeks. In both mice and hamsters, exposure to HCB increased the incidence of liver-cell tumours but no such tumours were observed in the controls. A significant increase in the incidence of thyroid tumours and liver haemangioendotheliomas was observed in hamsters treated with HCB. Our findings that HCB is carcinogenic in mice and hamsters, together with other results showing the same effect in rats, provide sufficient experimental evidence to recommend great caution in the use of this material.

Animals↗
PubMed1986

Influence of hexachlorobenzene on thyroids of male hamsters.

The effect of hexachlorobenzene (HCB) on thyroid function in hamsters was explored and compared with that of 3-amino-1,2,4-triazole. Both chemicals caused thyroid enlargement but whereas 3-amino-1,2,4-triazole depressed serum thyroxine (T4) levels and elevated triiodothyronine (T3), HCB depressed T3 with little effect on T4.

Animals↗
PubMed1985

Hepatocarcinogenicity of hexachlorobenzene in rats and the sex difference in hepatic iron status and development of porphyria.

Hexachlorobenzene (HCB) was fed to male and female F344 rats as 0.02% of the diet for 15 weeks. Females developed a massive porphyria, due to depression of uroporphyrinogen decarboxylase activity, whereas males did not. Although hepatic non-haem iron levels in control females were 3-5 times greater than males (iron is implicated in the pathogenesis of this condition) preloading the latter with iron did not increase their susceptibility. After 90 weeks of HCB treatment 100% of surviving females had multiple liver tumours which were strongly gamma-glutamyl transpeptidase (GGT) positive and histologically classified as neoplastic nodules or hepatocellular carcinomas. In contrast, only 16% of males developed tumours which were smaller and fewer in number per liver than those in females. Accumulation of porphyrins was still significantly less in males than females although no uroporphyrinogen decarboxylase activity was detected in treated livers of either sex. No differences in porphyrin levels or enzyme activity were found between tumours and surrounding tissue showing that tumours did not revert to a non-porphyric state. The sex difference in tumour response could not be explained by differences in hepatic HCB concentrations. Non-haem iron concentrations of livers fell after HCB treatment for 90 weeks in both sexes and were even lower in tumours. These studies demonstrate that not only are female rats far more sensitive than males to the porphyrinogenic effects of HCB but also to the hepatocarcinogenic actions, suggesting a link between these two manifestations of toxicity that may also apply to other polyhalogenated aromatics.

Animals↗
PubMed1984

A carcinogenicity study of styrene-7,8-oxide in rats.

Styrene-7,8-oxide (200 mg/kg body wt) was given orally to female BDIV rats on 17th day of pregnancy. Their offspring received 96 weekly doses of styrene oxide (100-150 mg/kg body wt). Following the continuous administration of styrene oxide, an increased incidence, statistically significant, of forestomach tumours was observed in rats of both sexes. The incidence of tumours occurring at other sites was similar in treated and control animals. The present results show that styrene oxide is a direct-acting carcinogen producing benign and malignant tumours of the forestomach.

Animals↗
PubMed1983

Testicular mesotheliomas in rats exposed to N-2-fluorenylacetamide (FAA).

The incidence of testicular mesotheliomas after exposure to the carcinogen N-2-fluorenylacetamide (FAA) was studied in Fischer 344 rats. The animals were fed a carcinogenic diet (containing 0.06% FAA) for 4 weeks and then a control diet for 1 week. This schedule was carried out for 3 complete cycles (12 weeks). A smaller group of rats was treated with FAA for 1 complete cycle only (4 weeks). One group of untreated controls was also available. The surviving rats were sacrificed at 59 weeks of age. The administration of FAA for 3 complete cycles resulted in a high incidence of liver, testis and Zymbal-gland tumors. The testicular tumours were mesotheliomas and occurred in 9/25 rats. No such tumour was observed in animals treated for 1 cycle only or in untreated controls. The high incidence of testicular mesotheliomas, a rare type of tumour in this and other rat strains, suggests an association with the treatment. The present experimental model may be useful in elucidating the mechanisms of the induction of mesothelial tumours of the testis by chemical carcinogens.

2-Acetylaminofluorene↗
PubMed1983

Carcinogenic effects induced in Wistar rats by combined treatment with technical-grade dichlorodiphenyltrichloroethane and sodium phenobarbital.

A group of 38 female and 39 male outbred Wistar rats were treated with 500 ppm technical-grade dichlorodiphenyltrichloroethane (DDT) in the diet and 500 ppm sodium phenobarbital (PB) dissolved in drinking-water for lifespan. Twenty-three of 29 (79.3%) female and 13/28 (46.4%) male surviving animals developed primary tumours which were detected starting at 65 weeks of age. Most of the liver tumours were neoplastic nodules, but well-differentiated hepatocellular carcinomas were also found in 3 males and 5 females of the exposed animals. No liver-cell tumour was observed in 59 rats exposed to a diet containing 3% olive oil.

Animals↗
PubMed1983

The inhibitory effects of ethoxyquin on the carcinogenic action of aflatoxin B1 in rats.

Ethoxyquin (EQ), a widely used antioxidant, inhibits the carcinogenic effects of polycyclic aromatic hydrocarbons. The aim of the present study was to determine whether EQ modifies the hepatocarcinogenic effects of aflatoxin B1 (AFB1) in rats. Both compounds were administered in the diet. Rats were fed either EQ for 2 weeks and then AFB1 for 6 weeks, EQ and AFB1 simultaneously or EQ following the cessation of AFB1 treatment. The results indicate that EQ can inhibit the hepatocarcinogenic effects of AFB1 and that the most effective inhibition is obtained when EQ and AFB1 are given simultaneously.

Aflatoxin B1↗
PubMed1983

Carcinogenicity study with technical-grade dichlorodiphenyltrichloroethane and 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene in hamsters.

Studies conducted by others have revealed that 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE), a proximal metabolite of dichlorodiphenyltrichloroethane (DDT), is a strong hepatocellular carcinogen in mice. Since hamsters appear to be resistant to tumor induction by DDT, we wanted to investigate whether DDE has any neoplastic effect in this species. DDE (99% pure) was mixed into the diet at doses of 500 or 1000 ppm and given to groups of male and female Syrian golden hamsters for life. Another group of animals received a diet containing 1000 ppm technical-grade DDT, and a further group served as control. Groups contained a minimum of 40 hamsters per sex. The tested compounds had no effect on the incidence of tumors at all sites, compared to controls. A specific finding in animals exposed to DDE was the appearance of hepatocellular tumors late in life. They were classified as neoplastic nodules, and the incidence was 15% in females and 47% in males of the 500-ppm DDE dose groups and 21% in females and 33% in males of the 1000-ppm DDE dose groups. None of the untreated or DDT-treated animals had these tumors. Eight animals treated with 1000 ppm DDE and four of those treated with DDT had hyperplastic foci of the liver. In addition, adrenocortical adenomas, spontaneous to Syrian golden hamsters, were more frequent in DDE- and DDT-treated animals than in control animals. These results showing that DDE, but not its parental compound, induces liver cell tumors in hamsters emphasize the importance of this metabolite as a proximal carcinogen of DDT.

Animals↗
PubMed1982

Lack of carcinogenicity of DDT in hamsters.

Syrian golden hamsters were fed for their lifespan a diet containing 0, 125, 250 and 500 parts per million (ppm) of ddt. The incidence of tumour bearing animals was 13% among control females and ranged between 11-20% in treated females. In control males 8% had tumours. The incidence of tumour bearing animals among treated males ranged between 17-28%. The incidence of adrenal cortex tumours showed a dose-related increase among the DDT-treated males. A liver-cell tumour and 2 liver hemangioendotheliomas were observed in 3 males treated with 250 ppm DDT. No liver-cell tumours were observed in the controls. No significant difference in tumour incidence was observed in treated versus control Syrian golden hamsters.

Adrenal Gland Neoplasms↗