Liver Function

Cornelius, Charles E.

doi:10.1016/b978-0-12-396350-5.50011-5

Cited by 49 publications

(43 citation statements)

References 156 publications

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“…There was a marked increase in the plasma bilirubin level, particularly of the conjugated type ( Table 2). Increase in plasma conjugated bilirubin level is a marker of cholestasis [26]. A similar increase in bilirubin level has been observed during hepatotoxicity and cholestasis in guinea pigs induced by lantana toxins [27,28].…”

Section: Discussionmentioning

confidence: 59%

Hepatotoxicity and cholestasis in rats induced by the sesquiterpene, 9‐oxo‐10,11‐dehydroageraphorone, isolated from Eupatorium adenophorum

Bhardwaj

Singh

Sharma

et al. 2001

J Biochem & Molecular Tox

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Eupatorium adenophorum leaves cause hepatotoxicity and cholestasis in rats. The hepatotoxicant has been characterized as 9-oxo-10,11-dehydroageraphorone (ODA), a cadinene sesquiterpene. Oral administration of ODA, mixed in feed to rats, caused jaundice in 24 h. The liver of the intoxicated animals had focal areas of hepatocellular necrosis, proliferation, and dilation of bile ducts with degenerative changes in the lining epithelium. There was marked increase in the conjugated form of plasma bilirubin and in the activities of the enzymes glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, alkaline phosphatase, lactate dehydrogenase, gamma-glutamyltranspeptidase, glutamate dehydrogenase, and 5'-nucleotidase. The histopathological lesions in liver and biochemical profile of marker enzymes show that ODA induced hepatotoxicity and cholestasis in rats. This is the first report on the toxicity of a cadinene sesquiterpene in rats.

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Section: Discussionmentioning

confidence: 59%

Hepatotoxicity and cholestasis in rats induced by the sesquiterpene, 9‐oxo‐10,11‐dehydroageraphorone, isolated from Eupatorium adenophorum

Bhardwaj

Singh

Sharma

et al. 2001

J Biochem & Molecular Tox

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“…There have been several reports that chronic hepatic disease is a common cause of hypoalbuminaemia and hypoproteinaemia in horses (Tennant and Hornbuckle 1980, Coffman 1981, Coles 1986, Duncan and Prasse 1986, Cornelius 1989, Kaneko 1989). However, the findings of this study, and of studies by Carlson (1982), Divers and others (1983) and Parraga and others (1995) provide no evidence of such an association.…”

Section: Resultsmentioning

confidence: 99%

Clinicopathological features of equine primary hepatic disease: a review of 50 cases

et al. 1999

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The clinicopathological features of 50 cases of equine hepatic disease were reviewed. There was a wide range of clinical signs and at least 50 per cent of the animals exhibited either dull demeanour, anorexia, abdominal pain, cerebral dysfunction and/or weight loss. Life-threatening complications of hepatic failure recorded were: gastric impaction in 10 cases, bilateral laryngeal paralysis in seven cases and coagulopathy in five cases. All the cases had high activities of gamma-glutamyl transferase (GGT) and most had high activities of glutamate dehydrogenase (GLDH) and high concentrations of bile acids. Fewer of the horses had abnormal concentrations of bilirubin, albumin and globulin. The horses that were euthanased or died had significantly higher concentrations of GGT, GLDH and bile acids than the survivors. There were biochemical data for 18 cases with signs of hepatic encephalopathy, all of them had plasma ammonia levels greater than 90 micromol/litre but this was not significantly correlated with the clinical severity of the condition. Half of the cases with hepatic encephalopathy were hyperglycaemic, none was hypoglycaemic, and none had abnormally low levels of plasma urea.

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“…To investigate whether urobilin (and its precursor form urobilinogen) is responsible for non-specific aggregation of particles, urobilinogen solutions were prepared, passively converted to urobilin (as it happens in typical urine samples within 24-h incubation time) (Cornelius, 1980), and added to the antibody-particles. Solutions of urobilinogen (catalog number 651-10, Lee Biosolutions) were prepared at concentrations of 2.5 mg/L and 0.75 mg/L, while the mean value of urobilinogen in 24-h urine is 0.71 mg/L (Kerkhoff and Peters, 1968), therefore representing high and normal urobilin concentrations.…”

Section: Mpad Filtration Of Urobilin From Urinementioning

confidence: 99%

“…Solutions of urobilinogen (catalog number 651-10, Lee Biosolutions) were prepared at concentrations of 2.5 mg/L and 0.75 mg/L, while the mean value of urobilinogen in 24-h urine is 0.71 mg/L (Kerkhoff and Peters, 1968), therefore representing high and normal urobilin concentrations. Both dilutions were exposed to ambient lighting at room temperature up to 24 h to induce in vitro oxidation of urobilinogen to urobilin (Cornelius, 1980). These solutions were added to anti-E. coli antibody-particles at 1:1 ratio, and incubated in a refrigerator (4°C) for 24 h. These mixtures were observed under the light microscope immediately after mixing and after 24-h incubation.…”

Section: Mpad Filtration Of Urobilin From Urinementioning

confidence: 99%

Smartphone-based, sensitive µPAD detection of urinary tract infection and gonorrhea

Cho

Park

Nahapetian

et al. 2015

Biosensors and Bioelectronics

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Liver Function

Cited by 49 publications

References 156 publications

Hepatotoxicity and cholestasis in rats induced by the sesquiterpene, 9‐oxo‐10,11‐dehydroageraphorone, isolated from Eupatorium adenophorum

Hepatotoxicity and cholestasis in rats induced by the sesquiterpene, 9‐oxo‐10,11‐dehydroageraphorone, isolated from Eupatorium adenophorum

Clinicopathological features of equine primary hepatic disease: a review of 50 cases

Smartphone-based, sensitive µPAD detection of urinary tract infection and gonorrhea

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