Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chlorozotocin was studied for toxic effects in beagle dogs and rhesus monkeys. The results are the subject of this report. The compound was administered i.v. as single and 5 daily doses in dogs and monkeys; and, in dogs, as 10 consecutive daily doses, once weekly for 6 weeks and for 5 daily doses followed by 9 days rest repeated 3 times. The most prominent toxicities in both species were dose-related renal tubular lesions. These appeared as a necrosis at the most toxic levels and a nephrosis at lower doses. The latter change was also seen in animals surviving higher doses but only after a 6-week posttreatment period. Bone marrow hypoplasia and lymphoid atrophy were other common findings at the highest doses in both species. The same general pattern of toxicity appeared in extended treatment studies in dogs, but also included aspermatogenesis. Signs of hepatotoxicity were seen in dogs at the highest dose levels, while monkeys receiving lethal doses also evidenced a toxic gastroenteritis. A single monkey had a diabetic response following 1 treatment with a high non-lethal dose. Renal lesions found in mice following acute, single dose administration were similar to those described for the larger laboratory animals.
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PMID:Toxicology studies in mice, beagle dogs and rhesus monkeys given chlorozotocin (NSC 178, 248). 15 61

Although plants containing hydrolysable tannins can be hepatotoxic, such poisoning has not been reported in Indonesia despite the presence of these plants. In order to determine the hepatotoxic potential of Indonesian plants, goats were intoxicated experimentally with the Indonesian plant Climedia hirta (harendong), which contained 19% hydrolysable tannin. The prophylactic effect of Ca(OH)2 supplementation on the disease was also examined. Two groups of goats were fed for 28 days with grain-based pellets containing 50% harendong leaf or 50% harendong leaf + 8% Ca(OH)2. Two control groups were fed similar pellets containing 50% of the non-toxic elephant grass (Pennisetum purpureum) with and without 8% Ca(OH)2. Serum enzymes indicative of liver damage were monitored during the experiment and histopathological examination of selected tissues was done at the conclusion of the experiment. In goats given unsupplemented harendong pellets there was a significant increase in aspartate aminotransferase and glutamate dehydrogenase from 50.2 and 20.6 U l-1 to 219.6 and 63.3 U l-1, respectively. These changes were associated with moderate to severe nuclear plemorphism, vacuolation and megalocytosis of hepatocytes and deposits of brown pigment in the Kupffer cells. There was also nephrosis of the renal convoluted tubules and collecting ducts, abomasitis and enteritis. Biochemical and histological changes were reduced significantly in the harendong + Ca(OH)2 group and virtually absent from control groups. It is concluded that hydrolysable tannins in harendong leaf are hepato- and nephrotoxic and associated with gastroenteritis, but that poisoning may be ameliorated by Ca(OH)2 supplementation.
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PMID:Prevention of hydrolysable tannin toxicity in goats fed Clidemia hirta by calcium hydroxide supplementation. 225 83

To focus attention on the problem of infant mortality in Lebanon, data were compiled on infant mortality from 1978 to 1986 at the American University of Beirut Medical Center. Causes of death are analyzed for 602 males and 398 females. 54.9% deaths occurred at 1 month of age and 77.4% died within the 1st year. Autopsies were performed on .7%. 37.7% of all neonatal deaths were due to neonatal diseases such as hyaline membrane disease, asphyxia neonatorum, immaturity, necrotizing enterocolitis, hemorrhage, hemolysis, meconium aspiration, and kernicterus. Better prenatal care would reduce this group, or the administration of corticosteroids to the mother 24-48 hours prior to delivery, as well as rapid resuscitation at birth and prevention of the 5 curses: hypoxemia, hypoglycemia, hypothermia, hypotension, and acidosis. Although unavailable in Lebanon, administration of surfactants through an endotracheal tube would also help. Infections constitute 25.1% of deaths; many are preventable through adequate public health measures and strict personal hygiene, i.e., diseases such as sepsis, pneumonia, meningitis, gastroenteritis, hepatitis, encephalitis, and 1-2 cases of the following: diphtheria, measles, peritonitis, tetanus, tuberculosis, cytomegalis inclusion, herpes, parathyphoid, pertussis, poliomyelitis, and shigellosis. Congenital diseases were 21.6%. In utero diagnosis could prevent some diseases and in utero treatment is possible for hydrocephalus and hydronephrosis. Screening programs postnatally could lead to treatment. 5.9% were malignancies such as leukemia, lymphoma, brain tumors, histocytosis, Wilm's tumor, Ewing sarcoma, and Hodgkin's disease. Early diagnosis is critical if mortality is to be reduced in this group, but medical advances are still needed. 2.9% are miscellaneous diseases such as poisoning, rheumatic diseases, marasmus, Reye's syndrome, nephrosis, rickets, and epilepsy. Most of these diseases are preventable, except for rheumatic inflammation of the heart. Recommended necessary steps to reduce infant mortality are: prenatal care, diagnosis and screening, intrauterine surgery; resuscitation and intensive care centers with modern equipment and trained personnel; national vaccination and screening programs; adequate public health measures and hygiene; parental education; and well-equipped hospitals to serve all regardless of income level.
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PMID:Pediatric mortality: an avoidable tragedy. 251 28

Two calves given a mean of 16.1 g and 16.4 g ripe Castanospermum australe seeds/kg body weight daily for 13 and 16 days respectively developed haemorrhagic gastroenteritis. The first calf died. The second calf had mild myocardial degeneration and necrosis and mild nephrosis at necropsy. Two calves given a mean of 16.8 g unripe C. australe seeds/kg body weight daily for 18 days remained clinically normal and had mild gastritis at necropsy. The activity of alpha-glucosidase was reduced in the mononuclear cells of peripheral blood and in skeletal muscle. This was attributed to the presence of the indolizidine alkaloid, castanospermine, in the seeds. The toxin causing the gastroenteritis and other lesions is unknown.
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PMID:The toxicity of Castanospermum australe seeds for cattle. 326 77

Five- to six-week-old crossbred pigs weighing 5 to 14 kg were given purified cyclopiazonic acid at dosages of 10, 1.0, 0.1, and 0.01 mg/kg body weight orally for 14 days. Clinical signs observed by day 7 in pigs given 10 mg/kg body weight were weakness, inactivity, anorexia, rough hair coats, and reduced body weights. These pigs also developed diarrhea during week 2 of the experiment. The pigs given 1.0 mg/kg body weight had rough hair coats and were moderately inactive during the second week of the experiment. At necropsy, lesions were observed only in pigs given 10 and 1.0 mg/kg body weight of cyclopiazonic acid. Lesions were gastric ulcers, mucosal hyperemia, and hemorrhage throughout the small and large intestine in pigs given 10 mg/kg body weight of cyclopiazonic acid. The pigs also had yellow, fibrononecrotic material in the lumen of the small intestine and pale livers. One pig given 1.0 mg/kg body weight had gastric ulceration. Microscopic lesions in pigs given 10 mg/kg body weight were necrotizing gastroenteritis, focal hepatocellular necrosis, hepatic peripheral lobular fatty change, and focal renal tubular nephrosis with focal suppurative tubulointerstitial nephritis. Pigs given 1.0 mg/kg body weight of cyclopiazonic acid had necrotizing gastritis and villous blunting in the jejunum and ileum.
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PMID:The toxicity of cyclopiazonic acid in weaned pigs. 646 2