Induction of glutathione S-transferases in genetically inbred male mice by dietary ethoxyquin hydrochloride

Makary, Moheb H.; Kim, H.L.; Safe, Stephen; Womack, James E.; Ivie, G. Wayne

doi:10.1016/0742-8413(89)90035-2

Cited by 6 publications

(4 citation statements)

References 19 publications

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“…In preneoplastic nodules of rat liver, the subunit 7-7 protein is strongly expressed (McLellan and Hayes 1987). Dietary factors, especially antioxidants such as butylated hydroxyanisole and ethoxyquin, have also been shown to induce hepatic GST activity (Makary et al 1989;Sparnins et al 1982). Plaice GST activity was induced by a variety of xenobiotics, including 3-methylcholanthrene and a polychlorinated biphenyl mixture (Arochlor) which act on the Ah locus, trans-stilbene oxide and ethoxyquin, a commonly utilised food antioxidant.…”

Section: Discussionmentioning

confidence: 99%

Isolation, properties and induction of plaice liver cytosolic glutathione-S-transferases

George

Buchanan

1990

Fish Physiol Biochem

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Three cytosolic glutathione S-transferases [E.C. 2.5.1.18] were identified in liver of a marine flatfish, the plaice (Pleuronectes platessa) and the two major isoforms were purified to homogeneity. There was no evidence for the presence of basic transferases. The plaice GST's exhibited comparable hematin binding to rat ligandin, however, bilirubin was only bound weakly and the enzymes did not display the inhibition characteristics of ligandin. They were extremely sensitive to inhibition by organotin compounds.Plaice transferase A was a homodimer of Mr 27 kDa subunits; it displayed strongest activity with CDNB and some activity with DCNB as substrates. Specific antibodies to it did not show any relationship with other plaice GST's or rat GST subunits 1,2,3,4,7,8 or 10. Plaice transferase B was a homodimer of Mr 25 kDa subunits, it displayed similar activities with CDNB and DCNB as substrates to transferase A and a low activity with ethacrynic acid or p-nitrobenzylchloride. It was immunologically related to the rat alpha class transferase subunits 1,2 and 8. A minor form, transferase AM, which was not separated from transferase A, appeared to be a heterodimer of Mr 25.5 and 27 kDa subunits. It displayed a greater activity with DCNB than the other plaice GST's and some activity with bromosulphalein indicative of a possible relationship with the Mu class transferases.

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Section: Discussionmentioning

confidence: 99%

Isolation, properties and induction of plaice liver cytosolic glutathione-S-transferases

George

Buchanan

1990

Fish Physiol Biochem

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“…Several enzymes involved in phase II metabolism of xenobiotics are induced by EQ, e.g., GST (3,14,31), UGT (4, 6), NADP(H):quinone oxidoreductase and epoxide hydrolase (27). UGT-mediated and sulfotransferase-mediated conjugation seem to be the major phase II pathways of EQ metabolism in rats and mice (11).…”

Section: Discussionmentioning

confidence: 98%

Investigations on the Metabolism and Potentially Adverse Effects of Ethoxyquin Dimer, a Major Metabolite of the Synthetic Antioxidant Ethoxyquin in Salmon Muscle

Ørnsrud¹,

Arukwe

Bohne

et al. 2011

Journal of Food Protection

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The feed additive ethoxyquin (EQ) is a commonly used synthetic antioxidant preservative in animal feeds. In farmed Atlantic salmon fillets, EQ residues are present, both as the parent compound and as EQ derivatives. One of the main EQ derivates in fish muscle is an ethoxyquin dimer (EQDM), and the potential toxicity of this metabolite is not known. The aim of this study was to evaluate the metabolism and potentially toxicological effects of EQDM. A 90-day subchronic exposure study with repeated dietary exposure to EQDM at 12.5 mg/kg of body weight per day was performed with male F344 rats. Hepatic Cyp1a1 mRNA was significantly reduced to <3% of the control in rats fed EQDM, and hepatic Cyp2b1 mRNA was increased to 192%. EQDM increased Gstpi1 mRNA expression to 144% that of the control, but the activity level of this phase II enzyme was reduced. Biomarkers of liver and kidney function did indicate adverse effects of EQDM when F344 rats were fed 12.5 mg/kg of body weight per day. The present study revealed that EQDM produces responses that are comparable to those produced by the parent compound (EQ) in terms of activating the same enzyme systems.

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“…Dietary administration of EQ (1) diminishes the neoplastic effects of a variety of chemicals (Wattenberg, 1980;Kahl, 1984), (2) induces hepatic glutathione (GSH) and glutathione S-transferases in rodents (Cha et al, 1982;Makary et al, 1989), and (3) protects animals from the toxic effects of pyrrolizidine alkaloids (Miranda et al, 1981), aflatoxin B, (Cabrai and Neal, 1983;Kensler et al, 1986), and other toxicants (Kim et al, 1982). EQ feeding has caused chronic glomerulonephrosis in rats that received a diet containing 0.5% EQ for 23 wk (Power et al, 1987).…”

Section: Introductionmentioning

confidence: 97%

Accumulation of ethoxyquin in the tissue

Kim

1991

Journal of Toxicology and Environmental Health

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Ethoxyquin (EQ) residue levels in the mouse tissue were determined by the HPLC-fluorometric detection method. Mice were given powdered feed containing 0, 0.125, and 0.5% EQ HCl and the EQ residue levels in liver, kidney, lung, and brain tissues were determined after 2, 4, 6, 10, and 14 wk (4 mice/group). The tissue samples were homogenized in 10 volumes (w/v) of acetonitrile-water (7:3, v/v), centrifuged, and the supernatants were stored in a freezer for 2-3 h or until the two layers separated; then the clear upper layers were analyzed. The mean EQ residue levels in the tissue ranged 0.84-4.58 micrograms EQ/g liver and 0.11-0.92 micrograms EQ/g brain. The relative weight of the liver (5.21-7.07% body weight) and the hepatic glutathione level (5.99-7.83 microM GSH/g tissue) of mice that received EQ were significantly higher than those of the controls (4.67-5.05% body weight and 4.30-5.78 microM GSH/g tissue, respectively). The mean hepatic mitochondrial glutathione level of the higher EQ feeding group, following dietary administration of EQ for 14 wk, was approximately twofold (1.68 nM GSH/mg protein) of both the control and the lower EQ feeding groups (0.83 and 0.74 nM GSH/mg protein, respectively).

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Induction of glutathione S-transferases in genetically inbred male mice by dietary ethoxyquin hydrochloride

Cited by 6 publications

References 19 publications

Isolation, properties and induction of plaice liver cytosolic glutathione-S-transferases

Isolation, properties and induction of plaice liver cytosolic glutathione-S-transferases

Investigations on the Metabolism and Potentially Adverse Effects of Ethoxyquin Dimer, a Major Metabolite of the Synthetic Antioxidant Ethoxyquin in Salmon Muscle

Accumulation of ethoxyquin in the tissue

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