PubMed Health⌕ Search

Biomedical subjects

R C Hatch

Publications and source records attributed to R C Hatch.

At least 55 records · Page 3Linked to original sources
PubMed1982

Effects of various treatments on induced chronic aflatoxicosis in rabbits.

Male New Zealand White rabbits were orally given 0.05 mg of aflatoxin B1 (AFB1)/kg of body weight daily for 10 days and were treated with glutathione-precursors and depletor, antibacterial agents, or sodium thiosulfate. The drug administered, the mortality, and the mean survival time were as follows: corn-oil controls (0), euthanatized at 25 days; AFB1-controls (2), 21 days; AFB1 and saline controls (2), 22 days; cysteine and AFB1 (5), 13 days; methionine and AFB1 (5), 12 days; sodium thiosulfate and AFB1 (2), 21 days; sulfadimethoxine and AFB1 (1), 24 days; oxytetracycline and AFB1 (0), euthanatized at 25 days; and ethyl maleate and AFB1 (3), 21 days. Clinical signs of toxicosis included decreased feed consumption during AFB1 administration, loss of body weight or failure to gain, and death. Clinicopathologic changes included increases in serum bilirubin concentration and alanine aminotransferase and aspartate aminotransferase activities. Prothrombin and activated partial thromboplastin times were lengthened. Plasma fibrinogen concentration was decreased. Changes in PCV, hemoglobin concentration, and serum alkaline phosphatase were unremarkable. Oxytetracycline had protective effects against chronic aflatoxicosis in rabbits. Cysteine and methionine enhanced chronic aflatoxicosis.

Aflatoxin B1↗
PubMed1982

Effect of some enzyme inducers, fluids, and methionine-thiosulfate on induced acute aflatoxicosis in goats.

Groups of four 6- to 12-month-old male goats were injected intraruminally with a lethal dose (3 mg/kg of body weight) of aflatoxin B1 (AFB1). Drugs were administered parenterally before (pretreatment) or beginning 8 hours after goats were doses with AFB1. These drugs were phenobarbital (PB), phenylbutazone (PBZ), piperonyl butoxide (PRO), benzoflavones, water, and 5% glucose solution (D5W). Most groups given the drugs after AFB1 was administered also were given intraperitoneal injections of methionine-sodium thiosulfate (MET-TS) solution. Clinical signs of toxicosis, serum aspartate aminotransferase activities, serum bilirubin concentrations, duration of illness, mortality, and gross and microscopic pathologic findings taken together indicated that toxicosis was increased with MET-TS + PB therapy, PBZ pretreatment, PBZ therapy, benzoflavone pretreatment, benzoflavone therapy, MET-TS + benzoflavone therapy, and MET-tS + water therapy. Toxicosis was not altered appreciably by MET-TS + PBO therapy. Beneficial effects (less severe toxicosis) were produced by PB pretreatment; these effects were prolonged maintenance of strength, vigor, and appetite and (in 1 goat that recovered) absence of pathologic changes or serum bilirubin increase. Therapy with MET-TS + D5W (but not MET-TS alone) also lengthened maintenance of strength, vigor, and appetite, but did not prevent pathologic changes. The beneficial effect of MET-TS therapy reported in a previous study (AFB2 dosage of 4 mg/kg) was not observed with the 3 mg/kg lethal dose. In conclusion, therapy for acute aflatoxicosis with inducers of hepatic microsomal enzymes is ineffective (PBO) or contraindicated (PB, PBZ, benzoflavones). Therapy with D5W may be a useful adjunct to other therapeutic drugs, but multiple intraperitoneal injections of D5W may decrease survival time because of stress.

Aflatoxin B1↗
PubMed1982

Effect of enzyme inducers and inhibitors and glutathione precursor and depleter on induced acute aflatoxicosis in rabbits.

Male New Zealand White rabbits were treated with microsomal enzyme inducers, inhibitors of hemoprotein synthesis or action, and glutathione precursor and depletor before they were orally given the median lethal dose (LD50) of aflatoxin B1 (AFB1; 0.4 mg/kg) at the start of a 7-day experimental period. The drugs administered, mean duration of illness (hours), and survival percentage were as follows: controls (saline solution)-85, 50%; phenobarbital (PB)-100, 100%; phenylbutazone-115, 67%; benzoflavone-39, 17%; stanozolol-67, 67%; cobaltous chloride (CoCl2)-46, 67%; piperonyl butoxide (PBO)-88, 100% cysteine (CYS)-68, 100%; ethyl maleate-71, 83%. Signs of toxicosis included decreased feed and water consumption, weight loss, dehydration, lethargy, and emaciation; some rabbits died or were euthanatized. Clinico-pathologic changes included increased serum aspartate aminotransferase (AST) activity by 24 hours and bilirubin concentration by 48 to 72 hours after AFB1 was given. Grossly, livers were pale or tan and friable, with prominent lobular architecture. Kidneys of affected rabbits were pale to dark red. Microscopically, livers were normal or had lesions as great as extensive necrosis, hemorrhage, mineralization, and bile duct proliferation. Treatment of rabbits with PB, CoCl2, PBO, and CYS protected against AFB1 hepatic pathology, and PB, PBO, and CYS also had protective effect against lethality. Ethyl maleate provided some protection against lethality and increased serum AST activity and bilirubin concentration. Toxicosis was enhanced by benzoflavone; phenylbutazone and stanozolol had litte influence.

Acute Disease↗
PubMed1982

Toxicologic study of carboxyatractyloside (active principle in cocklebur--Xanthium strumarium) in rats treated with enzyme inducers and inhibitors and glutathione precursor and depletor.

Male rats (10 rats/group) were treated with phenobarbital (PB), phenylbutazone (PBZ), stanozolol (3 inducers of cytochrome P450-dependent enzymes), piperonyl butoxide (PBO; a P450 inhibitor), cobaltous chloride (CoCl2; an inhibitor of hemoprotein synthesis), 5,6-benzoflavone (BNF; an inducer of cytochrome P448 dependent enzymes), cysteine [CYS; a glutathione (GSH) precursor], or ethyl maleate (EM; a GSH depletor). The rats were then given a calculated LD50 dosage (13.5 mg/kg of body weight) of carboxyatractyloside (CAT) intraperitoneally. Clinical signs of toxicosis, duration of illness, lethality, gross lesions, and hepatic and renal histopathologic lesions were recorded. Seemingly, (i) CAT toxicosis has independent lethal and cytotoxic components (PBZ decreased lethality and cytotoxicity; CoCl2 decreased cytotoxicity but not lethality; BNF decreased duration of illness, and perhaps lethality, but not cytotoxicity); (ii) CAT cytotoxicity could be partly due to an active metabolite formed by de novo-synthesized, P450-/P448-independent hemoprotein (PBZ and CoCl2 had anticytotoxic effects, but PB, stanozolol, PBO, and BNF did not); (iii) CAT detoxification may occur partly through a hemoprotein-independent, PBZ-inducible enzyme, and partly through a P448-dependent (BNF-inducible) enzyme; and (iv) CAT detoxification apparently is not P450 or GSH-dependent because PB, stanozolol, and CYS had no beneficial effects, and PBO, CoCl2, and EM did not enhance toxicosis. Metabolism of CAT may have a role in its cytotoxic and lethal effects.

Animals↗
PubMed1981

Abnormal concentrations of B vitamins and amino acids in plasma and B vitamins in bile of rabbits with aflatoxicosis.

The dosages of aflatoxin B1 (AFB1) required to produce significant changes in concentrations of B vitamins in plasma and bile and of amino acids in plasma of rabbits were determined. Folate increased by 98% in plasma, whereas concentration of thiamine, vitamin B6, and biotin decreased by more than 50%. In bile, choline and biotin increased 14- and 18-fold, respectively, whereas folate and niacin decreased by more than 50%. All amino acids in plasma increased between 76 and 155%. The dosages of AFB1 required to induce these changes were usually between 12.5 and 37.5 microgram/kg of body weight per day. Except for changes in biliary concentrations of pantothenic acid, folic acid, and biotin, lower threshold dosages of aflatoxin were required to produce weight loss and anorexia (5.0 and 8.5 microgram of AFB1/kg per day, respectively) than for changes in vitamins and amino acids (approximately 25 to 50 microgram of AFB1/kg per day). The data indicated that AFB1 interfered with the metabolism of B vitamins and amino acids in rabbits.

Aflatoxin B1↗
PubMed1980

Determination of aflatoxins in compound feedstuffs containing citrus pulp.

A method is described for determining aflatoxins B1, B2, G1, and G2 in compound feedstuffs containing citrus pulp. A finely ground sample is extracted with methylene chloride in a blender and cleaned with lead acetate. An aliquot of the cleaned extract is partitioned into methylene chloride and evaporated to dryness. The residue is dissolved in 0.5 mL chloroform. A 10 muL sample is applied to a thin layer chromatographic (TLC) plate and developed in 2 dimensions. Aflatoxins B1, B2, G1, and G2 are resolved and quantitated visually. The average recoveries were 96, 104, 98, and 102%, respectively. As little as 5 micrograms aflatoxin B1 or G1/kg, and 1.5 micrograms aflatoxin B2 or G1/kg can be determined by this procedure.

Aflatoxins↗