Object
Title: Effect of cocaine on the metabolism of endogenous sulfur compounds in rats
Abstract:
Cocaine is one of the most widely used and highly addictive drugs. Previous cocaine studies evaluated its effect on the central nervous system, however multiorgan toxicity of this drug has also been documented. This thesis is the first report of the effect of cocaine on metabolism of thiol compounds in peripheral organs. The aim of the presented work was to examine the effect of cocaine on thiol redox status, anaerobic and aerobic cysteine metabolism and oxidative stress in the liver, kidney and plasma of Zał. nr 1 do § 2 zarządzenia nr 45 Rektora UJ z 12 czerwca 2006 roku rats. Two models of cocaine administration were used: acute and chronic intraperitoneal administration and intravenous self-administration during cocaine exposure or withdrawal. The studies clearly demonstrated a significant role of cocaine in the generation of changes in cysteine metabolism. It was shown that cocaine shifted this metabolism towards the anaerobic route which led to overproduction of sulfane sulfur and H2S. The presented research also revealed differences in the effects of cocaine on certain thiol redox forms between animals actively self-administering the drug and those passively receiving cocaine which suggests that motivational aspect is an important factor determining the influence of cocaine. It was also shown that cocaine altered the activity and expression of enzymes participating ; in synthesis of reactive sulfur species. These changes differed depending on the tissue and administration paradigm what suggests that thiol redox regulation plays an important role in pharmacological and motivational actions of cocaine.
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Degree grantor:
Rada Dyscypliny Nauki farmaceutyczne
Promoter:
Lorenc-Koci, Elżbieta ; Iciek, Małgorzata
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Last modified:
Mar 22, 2024
In our library since:
Jan 27, 2023
Number of object content hits:
6
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0
All available object's versions:
http://dl.cm-uj.krakow.pl:8080/publication/4940
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| Edition name | Date |
|---|---|
| ZB-136387 | Mar 22, 2024 |
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