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Biomedical subjects

C C Chou

Publications and source records attributed to C C Chou.

At least 181 records · Page 10Linked to original sources
PubMed1976

Experimental acute aflatoxicosis in mink (Mustela vison).

Susceptibility of mink to intoxication by aflatoxins was studied by giving mink single doses (300, 600, and 900 mug of aflatoxins B1 and G1 (40:60)/kg of body weight) and observing them for 8 weeks. One, 2, and 4 of 5 mink in each group died within 4 days after ingesting the small, medium, and large doses, respectively. Enlarged liver with pale yellow to yellowish pink spots was the most consistent lesion observed in mink that died of acute aflatoxicosis. Some lobules of liver also appeared hemorrhagic and fragile, whereas others showed fatty metamorphosis. Histopathologic examination of the liver showed different degrees of fat infiltration, bile duct proliferation, and necrosis of liver cells. Hematologically, mink that survived were not appreciably different from control mink in terms of hemoglobin content, packed cell volume, and white blood cell count. Liver specimen from aflatoxin-treated mink contained more fat, was larger, and contained less protein, RNA and DNA than did liver from control mink. Aflatoxin residue (only B1 ) was recovered from liver of 6 mink and were between 0.1 and 7.6 mug of the original dose.

Animals↗
PubMed1976

Mortality and some biochemical changes in mink (Mustela vison) given sublethal doses of aflatoxin each day.

Two feeding trials were done to study the susceptibility of mink (Mustela vison) to multiple sublethal doses of aflatoxins. In the 1st trial, twenty 3-month-old male mink were divided equally among groups. Each mink in groups 1, 2, 3, and 4 was given a meatball daily that contained 15, 30, 45, or 0 mug of aflatoxins (B1:G1, 40:60), respectively. All mink in group 3 died between the 25th and the 30th days of the feeding trial. Each mink had ingested 1,035 to 1,480 mug of aflatoxins. Four of the mink in group 2 died almost as soon as did mink in group 3. Four mink in group 1 died between 40 and 59 days after the start of the feeding trial. Generally, a marked increase in plasma cholesterol and alkaline phosphatase activity appeared before mink died. The liver from animals that died of aflatoxicosis showed prominent pathologic changes which included hemorrhages and appearance of pink yellow spots. Histopathologic examination of liver from dead mink revealed fatty infiltration, bile duct proliferation, bile stasis, pseudotubular formation, congestion, and fibrosis. The feeding trial was repeated with 20 mink (8 males and 12 females) that were 1.5 to 2 years old. In this instance, 0, 20, 40, and 60 mug of aflatoxins were administered each day. All treated animals, except 1, were dead within 37 days after the experiment started. The survivor was given the lowest dosage of toxins and died after 52 days by which time 960 mug of aflatoxins were consumed. Plasma cholesterol content and alkaline phosphatase activity generally were similar to those observed in younger mink of the 1st feeding trial.

Aflatoxins↗
PubMed1976

Growth of mink (Mustela vison) kits when nursing dams given aflatoxin G1.

During lactation, 5 female mink (Mustela vison) were given 50 mug of aflatoxin B1 orally twice, 2 weeks apart. Another group of 5 lactating mink were used as controls, Milk was collected 24 hours after each treatment with toxin. Aflatoxin B1 and M1 could not be detected in the milk. There was no appreciable difference in body weight among kits that nursed treated mink and those that nursed untreated mink.

Aflatoxins↗
PubMed1975

Incorporation of (2-14C)acetate into lipids of mink (Mustela vison) liver and intestine during in vitro and in vivo treatment with aflatoxin B1.

The in vitro and in vivo incorporation of (2-14C)acetate into lipids of mink (Mustela vison) liver and intestines was studied. In vitro, a dose of aflatoxin B1 as small as 7.5 mug/ml of medium reduced by 20% the amount of (2-14C)acetate incorporated into lipids of mink liver slices, whereas 180 mug caused 76% reduction in the synthesis of lipids from the radioactive precusor. Similar inhibition of lipid synthesis by aflatoxin also was observed with tissues from mink intestines and fatty liver. The degree of inhibition (19 to 84% for tissue from intestines and 19 to 64% for tissue from fatty livers) depended on the amount of aflatoxin B1 (7.5 TO 180 MUG) present in the medium. In vivo, a substantially increased amount of 14C-labeled lipids was found in the livers of mink injected with 600 mug of aflatoxin B1 per kg of body weight 20, 28, and 40 h earlier. However, no appreciable difference in incorporation of (2-14C)acetate into lipids was observed between toxin-treated and control animals when these animals were sacrificed and examined for 14C-labeled lipids at 4 and 10 h after toxin was administered.

Acetates↗
PubMed1975

Distribution of blood flow in the intestine with hypertonic glucose in the lumen.

The effects of luminal placement of 50 percent glucose solution on distribution of blood flow within the jejunal wall were studied with radioactive microspheres. Two types of spheres, 15 +/- 5 mu in diameter, were used. One was labeled with cerium- 141 (Ce- 141) and the other with strontium-85 (Sr-85). They were injected sequentially to test for reproducibility of the results. These two types of spheres gave similar results qualitatively and quantitatively. Luminal placement of 50 percent glucose increased total blood flow to the jejunal wall but the increase occurred mainly in the mucosal layer. The flow to the submucosa or muscularis-serosa was not altered. This increased mucosal flow was attenuated by prior exposure of the mucosa to a local anesthetic, dibucaine. It is suggested that the increased intestinal blood flow that occurs in the experimental dumping syndrome is confined to the mucosa of the intestine and is mediated by mechanisms that can be inhibited by exposing the mucosa to a local anesthetic.

Anesthesia, Local↗