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Title: Various studies on liver disease
Author: Patrick, Robert S.
Awarding Body: University of Glasgow
Current Institution: University of Glasgow
Date of Award: 1961
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1. Liver necrosis was produced in mice by the oral administration of bromobenzene following a short period of starvation. The lesion consisted of centrilobular or mid-zonal necrosis and a variable degree of massive necrosis. 2. Autoradiographs were prepared from liver sections following the intraperitoneal injection of S35-methionine and S35-cystine. The maximum sites of liver damage induced by bromobenzene were not depleted of either amino-acid, but there appeared to be some loss from periportal hepatic tissues which remained viable. 3. As a similar result was obtained with carbon tetrachloride, it may be that those changes detected by autoradiography are not specific for bromobenzene poisoning, although this substance is alleged to damage the liver by the removal of sulph-hydryl compounds. 4. S35-methionine given to mice already suffering from bromobenzene or carbon tetrachloride poisoning was taken up mainly by viable periportal hepatic tissue. By contrast, S35-cystine was taken up preferentially by damaged or necrotic tissue. 5. Fatty liver was produced in young female rats by the administration of dl-ethionine over a twelve-hour period, following a brief spell of starvation. Autoradiography showed no loss of S35-methionine or S-cystine in such cases. 6. Quantitation of radio-activity in liver sections, using a gas-flow counter, failed to show a correlation with the autoradiographic findings. This was probably due to errors in the assessment of the masses of tissue so analysed. 7. These results are discussed in relation to ourrent knowledge concerning the role of sulphur-containing amino-acids in liver disease. It would appear that: (a) ethionine may interfere with the methyl-donating role of methionine and cause fatty liver without depleting the tissues of organic sulphur-containing compounds; (b) liver necrosis in bromobenzene poisoning may depend on factors other than depletion of sulphur-containing amino-acids. Recent work on dietary liver necrosis has shown that the absence of these amino-acids may be unimportant in the production of liver damage.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (M.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available