scholarly journals The changes in hepatic enzyme expression caused by selenium deficiency and hypothyroidism in rats are produced by independent mechanisms

1990 ◽  
Vol 266 (3) ◽  
pp. 743-747 ◽  
Author(s):  
G J Beckett ◽  
F Nicol ◽  
D Proudfoot ◽  
K Dyson ◽  
G Loucaides ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Malic Enzyme ◽  
Selenium Deficiency ◽  
Hepatic Enzyme ◽  
Enzyme Expression ◽  
Glutathione S Transferase ◽  
Plasma Enzymes ◽  
Glycerophosphate Dehydrogenase ◽  
Se Deficiency ◽  
Gst Activity

Selenium (Se) deficiency for 5 weeks in rats produced changes in the activity of a number of hepatic, renal and plasma enzymes. In animals whose food intake was restricted to 75% of normal for 2 weeks, Se deficiency produced significant increases in the activity of hepatic cytosolic ‘malic’ enzyme and mitochondrial alpha-glycerophosphate dehydrogenase (GPD), two enzymes that are particular sensitive to the thyroid-hormone concentrations in tissue. Propylthiouracil-induced hypothyroidism produced significant decreases in ‘malic’ enzyme and GPD activities. The effect of hypothyroidism on the activity of ‘malic’ enzyme, GPD and other enzymes studied in liver and plasma was often opposite to that seen in Se deficiency. Glutathione S-transferase (GST) activity was increased by both Se deficiency and hypothyroidism, but in hypothyroid animals further significant increases in GST were produced by Se deficiency. These data suggest that the changes in enzyme expression observed in Se deficiency are not caused by decreased tissue exposure to thyroid hormones.

scholarly journals Effect of selenium deficiency on hepatic type I 5-iodothyronine deiodinase activity and hepatic thyroid hormone levels in the rat

1992 ◽  
Vol 282 (2) ◽  
pp. 483-486 ◽  
Author(s):  
G J Beckett ◽  
A Russell ◽  
F Nicol ◽  
P Sahu ◽  
C R Wolf ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Selenium Deficiency ◽  
Type I ◽  
Hepatic Enzymes ◽  
Glutathione S Transferase ◽  
Iodothyronine Deiodinase ◽  
Hepatic Glutathione ◽  
Liver Homogenates ◽  
Thyroid Hormone Levels ◽  
Gst Activity

Selenium deficiency in rats for a period of up to 6 weeks inhibited both the production of 3,3′, 5-tri-iodothyronine (T3) from thyroxine (T4) (5′-deiodination) and also the catabolism of T3 to 3,3′-di-iodothyronine (5-deiodination) in liver homogenates. The hepatic stores of T3 were decreased by only 8% in selenium deficiency, despite the T3 production rate from T4 being only 7% of the rate found in selenium-supplemented rats. Hepatic glutathione S-transferase (GST) activity was increased in both hypothyroidism and selenium deficiency, but apparently by different mechanisms, since mRNA expression for this family of enzymes was lowered by hypothyroidism and increased in selenium deficiency. It is concluded that, since both T3 production and catabolism are inhibited by selenium deficiency, there is little change in hepatic T3 stores, and therefore the changes in the activity of certain hepatic enzymes, such as GST, that are found in selenium deficiency are not the result of tissue hypothyroidism.

scholarly journals The effects of selenium and copper deficiencies on glutathione S-transferase and glutathione peroxidase in rat liver

1987 ◽  
Vol 248 (2) ◽  
pp. 539-544 ◽  
Author(s):  
J R Arthur ◽  
P C Morrice ◽  
F Nicol ◽  
S E Beddows ◽  
R Boyd ◽  
...  
Keyword(s):  
Glutathione Peroxidase ◽  
Glutathione Peroxidase Activity ◽  
Glutathione S Transferase ◽  
Similar Extent ◽  
Compensatory Response ◽  
Cu Deficiency ◽  
Hepatic Glutathione ◽  
Gshpx Activity ◽  
Se Deficiency ◽  
Gst Activity

Selenium (Se) deficiency in rats produced significant increases in the activity of hepatic glutathione S-transferase (GST) with 1-chloro-2,4-dinitrobenzene as substrate and in various GST isoenzymes when determined by radioimmunoassay. These changes is GST activity and concentration were associated with Se deficiency that was severe enough to provoke decreases of over 98% in hepatic Se-containing glutathione peroxidase activity (Se-GSHpx). However, decreases in hepatic Se-GSHpx of 60% induced by copper (Cu) deficiency had no effect on GST activity or concentration. Increased GST activity in Se deficiency has previously been postulated to be a compensatory response to loss of Se-GSHpx, since some GSTs have a non-Se-glutathione peroxidase (non-Se-GSHpx) activity. However, the GST isoenzymes determined in this study, GST Yb1Yb1, GST YcYc and GST YaYa, are known to have up to 30-fold differences in non-Se-GSHpx activity, but they were all significantly increased to a similar extent in the Se-deficient rats.

Chemoprotective Effects of Propolis on Aflatoxin B1-Induced Hepatotoxicity in Rats: Oxidative Damage and Hepatotoxicity by Modulating TP53, Oxidative Stress

2020 ◽  
Vol 17 (3) ◽  
pp. 191-199
Author(s):  
Seval Yilmaz ◽  
Fatih Mehmet Kandemir ◽  
Emre Kaya ◽  
Mustafa Ozkaraca
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Oxidative Damage ◽  
Aflatoxin B1 ◽  
Tp53 Gene ◽  
Control Group ◽  
Glutathione S Transferase ◽  
Gene Expressions ◽  
Cat Gene ◽  
Gst Activity

Objective: This study aimed to detect hepatic oxidative damage caused by aflatoxin B1 (AFB1), as well as to examine how propolis protects against hepatotoxic effects of AFB1. Method: Rats were split into four groups as control group, AFB1 group, propolis group, AFB1+ propolis group. Results: There was significant increase in malondialdehyde (MDA) level and tumor suppressor protein (TP53) gene expression, Glutathione (GSH) level, Catalase (CAT) activity, CAT gene expression decreased in AFB1 group in blood. MDA level and Glutathione-S-Transferase (GST) activity, GST and TP53 gene expressions increased in AFB1 group, whereas GSH level and CAT activity alongside CAT gene expression decreased in liver. AFB1+propolis group showed significant decrease in MDA level, GST activity, TP53 and GST gene expressions, GSH level and CAT activity and CAT gene expression increased in liver compared to AFB1 group. Conclusion: These results suggest that propolis may potentially be natural agent that prevents AFB1- induced oxidative stress and hepatotoxicity.

scholarly journals Inhibition of hepatic deiodination of thyroxine is caused by selenium deficiency in rats

1987 ◽  
Vol 248 (2) ◽  
pp. 443-447 ◽  
Author(s):  
G J Beckett ◽  
S E Beddows ◽  
P C Morrice ◽  
F Nicol ◽  
J R Arthur
Keyword(s):  
Thyroid Hormones ◽  
Production Rate ◽  
Selenium Deficiency ◽  
Enzyme Complex ◽  
Measurable Effect ◽  
Direct Role ◽  
Mechanism Of Inhibition ◽  
Se Deficiency

Selenium (Se) deficiency produced up to a 14-fold decrease in hepatic tri-iodothyronine (T3) production from thyroxine (T4) in vitro. The T3 production rate could not be restored by the addition of a variety of cofactors, nor by the addition of control homogenate. The impairment in hepatic T3 production observed in Se deficiency was reflected in the concentrations of thyroid hormones circulating in plasma, T4 being increased approx. 40% and T3 being decreased by 30%. However, the fall in plasma T3 concentrations was smaller than might be expected in view of the marked decreased in T3 production. Se deficiency had no measurable effect on plasma reverse-tri-iodothyronine concentrations. The data suggest that Se deficiency produces an inhibition of both 5- and 5′-deiodination, consistent with the widely held view that these reactions are catalysed by the same enzyme complex. The mechanism of inhibition appears not be mediated by changes in thiol levels, but a direct role of Se in the activity of the deiodinase complex cannot be excluded.

Sign in / Sign up

Export Citation Format

Share Document