The effect of oleic and palmitic acid on induction of steatosis and cytotoxicity on rat hepatocytes in primary culture

Title:

The effect of oleic and palmitic acid on induction of steatosis and cytotoxicity on rat hepatocytes in primary culture

Creator:

Moravcová, A., Zuzana Červinková, Otto Kučera, Mezera, V., Rychtrmoc, D., and Halka Lotková

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:8969fa6f-b43a-4438-ad66-d727ec209e27
uuid:8969fa6f-b43a-4438-ad66-d727ec209e27
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, apoptóza, apoptosis, steatosis, palmitic acid, oleic acid, cytotoxicity, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

In vitro models serve as a tool for studies of steatosis. Palmitic and oleic acids can induce steatosis in cultured hepatocytes. The aim of our study was to verify steatogenic and cytotoxic effects of palmitic acid (PA), oleic acid (OA) and their combinations as well as their impact on functional capacity of rat primary hepatocytes. Hepatocytes were exposed to OA or PA (0.125-2 mmol/l) or their combination at ratios of 3:1, 2:1 or 1:1 at the final concentrations of 0.5-1 mmol/l. Both OA and PA caused a dose-dependent increase in triacylglycerol content in hepatocytes. PA was more steatogenic at 0.25 and 0.5 mmol/l while OA at 0.75 and 1 mmol/l. PA exhibited a dose-dependent cytotoxic effect associated with ROS production, present markers of apoptosis and necrosis and a decrease in albumin production. OA induced a damage of the cytoplasmic membrane from 1 mM concentration. Mixture of OA and PA induced lower cytotoxicity with less weakened functional capacity than did PA alone. Extent of steatosis was comparable to that after exposure to OA alone. In conclusion, OA or combination of OA with PA is more suitable for simulation of simple steatosis than PA alone., A. Moravcová, Z. Červinková, O. Kučera, V. Mezera, D. Rychtrmoc, H. Lotková., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2015 Volume:64 | Number:Suppl 5

Harvested from:

CDK

Metadata only:

false