The effects of selenium and copper deficiencies on glutathione <i>S</i>-transferase and glutathione peroxidase in rat liver

Arthur, John R.; Morrice, Philip C.; Nicol, Fergus; Beddows, S E; Boyd, R; Hayes, John D.; Beckett, G J

doi:10.1042/bj2480539

Cited by 61 publications

(22 citation statements)

References 28 publications

(31 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The current study demonstrates that endogenous factors generated in i o by oxidative stress induced by I\R increase the expression of rGSTA1\A2. In other studies in i o it was found that oxidative stress secondary to selenium deficiency or generated by exercise also increased the expression of rGSTA1\A2 [39][40][41]. Therefore increases in the hepatic expression of some alpha class GSTs are a consistent feature of oxidative stress both in i o and in itro.…”

Section: Discussionmentioning

confidence: 88%

Ischaemia and reperfusion injury of rat liver increases expression of glutathione S-transferase A1/A2 in zone 3 of the hepatic lobule

Branum

Selim

Liu

et al. 1998

Biochemical Journal

View full text Add to dashboard Cite

Effects of ischaemia-reperfusion injury (I\R) of liver on expression of rat glutathione S-transferase (rGST) isoenzymes that metabolize products of oxidative stress were examined. Rats underwent lobar liver ischaemia for 30 min followed by reperfusion. In ischaemic lobes, rGSTA1\A2 transcript levels increased significantly 12 h after I\R (2.94-fold) and protein levels increased significantly at 24 h (1.45-fold) ; increased transcript levels were also observed in nonischaemic lobes (1.78-fold). Superoxide dismutase prevented I\R and the increases in transcript and protein levels in ischaemic and non-ischaemic lobes.

show abstract

Section: Discussionmentioning

confidence: 88%

Ischaemia and reperfusion injury of rat liver increases expression of glutathione S-transferase A1/A2 in zone 3 of the hepatic lobule

Branum

Selim

Liu

et al. 1998

Biochemical Journal

View full text Add to dashboard Cite

show abstract

“…Glutathione peroxidase activity in homogenates prepared from 0.5 cm colon segments ( n = 3) was determined using a glutathione reductase coupled assay with 0.25 mM H 2 O 2 and 5 mM glutathione as substrates [18]. A unit of cytosolic glutathione peroxidase is defined as that which oxidises 1 μmol of NADPH per min.…”

Section: Methodsmentioning

confidence: 99%

Novel sites of cytosolic glutathione peroxidase expression in colon

Drew¹,

Farquharson²,

Arthur³

et al. 2005

FEBS Letters

View full text Add to dashboard Cite

Glutathione peroxidases (Gpx) are important moderators of oxidative stress that is implicated in the pathogenesis of numerous diseases including colon cancer. Previous studies report limited examinations of cytosolic glutathione peroxidase location of expression in colon tissue. This study reports evidence of both common sites of Gpx1 and Gpx2 expression in rat colon and sites that are exclusive to each isoform. Semi-quantitative PCR performed previously demonstrated RNA expression of Gpx1 and Gpx2 in proximal, transverse and distal colon. Mapping the distribution throughout the entire colon has revealed specific, novel sites of glutathione peroxidase expression in colon lymphatic tissue. In situ hybridisation and immunohistochemistry confirmed micro-anatomical location of Gpx1 within lymphatic tissue and the lamina propria, sub-mucosa, muscularis and serosa, but not the lumenal epithelium. In situ hybridisation and immunohistochemistry were consistent with reports of microanatomical location of Gpx2 in the lumenal epithelium. Novel sites of Gpx2 expression were also observed in lymphatic tissue. Immunolocalisation in the vicinity of aberrant crypt foci was also examined to further investigate the link between glutathione peroxidases and colon cancer. This did not reveal significant abnormalities, nor did measurement of cytosolic glutathione peroxidase activity or gene expression in colon tissue from rats treated with the colontropic chemical, 1,2-dimethylhydrazine. These results support the potential for Gpx1 and Gpx2 redundancy in lymphatic tissue, but not in epithelial cells of the colon crypt or in the lamina propria, sub-mucosa, muscularis or serosa.

show abstract

“…The GSTs are a group of dimeric enzymes with several biochemical functions, the most important of which is probably detoxification. The major GST subunits in the rat are Ya, Yb1, Yb2 and Yc; the Ya and Yc subunits belong to the Alpha class and the Yb1 and Yb2 subunits belong to the Mu class [11,121. Using specific radioimmunoassay we have shown that Se deficiency increases the hepatic content of each of these subunits [13]. Rat liver also contains small amounts of the Yf subunit of the Pi class, but this subunit has been shown by immunohistochemistry to be present in the biliary epithelia and not the hepatocyte.…”

Section: Introductionmentioning

confidence: 93%

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

Beckett

Russell²,

Nicol³

et al. 1992

Biochemical Journal

Self Cite

View full text Add to dashboard Cite

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.

show abstract

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

Cited by 61 publications

References 28 publications

Ischaemia and reperfusion injury of rat liver increases expression of glutathione S-transferase A1/A2 in zone 3 of the hepatic lobule

Ischaemia and reperfusion injury of rat liver increases expression of glutathione S-transferase A1/A2 in zone 3 of the hepatic lobule

Novel sites of cytosolic glutathione peroxidase expression in colon

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

Contact Info

Product

Resources

About