Iron depletion prevents adenine nucleotide decomposition and an increase of xanthine oxidase activity in the liver of the Long Evans Cinnamon (LEC) rat, an animal model of Wilson's disease

Sakata, Naoki; Ohta, Tatsuro; Lai, Yurong; Sugawara, Chieko; Yuasa, Motoyuki; Nakamura, Masao; Tamura, Mamoru

doi:10.1016/s0024-3205(99)00378-1

Cited by 18 publications

(11 citation statements)

References 19 publications

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“…All of these observations are consistent with the model that copper status can modulate iron release due to the metal's regulation of FPN1 gene expression. This model is also consistent with the observations that copper-deficient rodents, which have ironloaded but copper-depleted livers, display profound microcytic anemia (5, 6), whereas Cp Ϫ/Ϫ mice and ceruloplasmindeficient Long-Evans Cinnamon rats, which have hepatic iron-and copper-loading, suffer only mild hematological disturbances (10,11,40).…”

Section: Discussionsupporting

confidence: 89%

Copper-induced ferroportin-1 expression in J774 macrophages is associated with increased iron efflux

Chung

Haile²,

Wessling‐Resnick

2004

Proc. Natl. Acad. Sci. U.S.A.

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Copper is known to play a role in iron recycling from macrophages. To examine whether cellular copper status affects expression of the iron exporter ferroportin-1 (FPN1), J774 macrophage cells were exposed to 10 -100 M CuSO4 for up to 20 h. Copper treatment significantly increased FPN1 mRNA in a dose-and time-dependent manner. After 20 h, 100 M CuSO4 up-regulated FPN1 transcript levels Ϸ13-fold compared to untreated controls. Induction was detected 8 h after copper treatment was initiated and markedly increased thereafter. A corresponding increase in FPN1 protein levels was observed upon copper treatment. Induction of J774 cell FPN1 expression by copper was also associated with a dosedependent increase in 59 Fe release after erythrophagocytosis of labeled red blood cells. Thus, a previously uncharacterized role for copper in the regulation of macrophage iron recycling is suggested by the induction of FPN1 gene expression and iron efflux by this metal.

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Section: Discussionsupporting

confidence: 89%

Copper-induced ferroportin-1 expression in J774 macrophages is associated with increased iron efflux

Chung

Haile²,

Wessling‐Resnick

2004

Proc. Natl. Acad. Sci. U.S.A.

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“…But the inhibitions on liver XOD activity of flavonoids observed at higher dose (55. 26,59.65, 43.86, 39.47%) were much weaker than that of allopurinol. However, apigenin failed to inhibit liver XOD activity.…”

Section: Hypouricemic Action In Hyperuricemic Micementioning

confidence: 88%

“…25,26) Briefly, XOD activity was determined in a 50 mM potassium phosphate buffer, pH 8.0 containing 1 mM EDTANa with the presence of 100 mM xanthine as the substrate. The mixture was incubated at 37°C for 30 min.…”

Section: Hypouricemic Action Of Selected Flavonoids In Mice: Structurmentioning

confidence: 99%

Hypouricemic Action of Selected Flavonoids in Mice: Structure-Activity Relationships

Zhou

et al. 2007

Biological & Pharmaceutical Bulletin

154

104

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Gout occurs in individuals who have high serum uric acid levels, in response to precipitation of monosodium urate monohydrate crystals in various tissues, followed by an inflammatory response. 1) The essence of the prevention and treatment of gout is antihyperuricemic therapy, either by uricosuric drugs or by xanthine oxidase (XOD) inhibitors. Allopurinol, an XOD inhibitor which is structurally related to xanthine, binds tightly to the active site of XOD thus causes inhibition on XOD. Allopurinol is used to treat gout for more than 40 years and remains a cornerstone in the therapy of primary and secondary hyperuricemia. 2-7) However, the most common adverse effects of allopurinol are gastrointestinal distress, hypersensitivity reactions, 8) and renal toxicity. 9) Thus, new alternatives with an increased therapeutic activity and less side effects are desired.Dietary flavonoids have been attracted attention because of their potential beneficial effects on human health. The structural components common to these molecules include two benzene rings on either side of a 3-carbon ring (Table 1). 10) Multiple combinations of hydroxyl groups, sugars, oxygens, and methyl groups attached to these structures create the various classes of flavonoids: flavanols, flavanones, flavones, flavanonol, flavan-3-ols (catechins), anthocyanins, and isoflavones. 11) Flavonoids are well known to possess antiviral, antiallergic, antiplatelet, antiinflammatory, antitumor and antioxidant activities. 12-15) Catechin and its derivatives, oligomeric proanthocyanidins, quercetin and quercetin chalcone, Ginkgo flavone glycosides, silymarin, and others can be utilized in preventative and treatment protocols for cardiovascular disease, cancer, inflammatory conditions, asthma, periodontal disease, liver disease, cataracts and macular degeneration. 16,17) Hyperuricemia is a risk factor for the disorder metabolic syndrome and increased cardiovascular disease, and the mechanisms involve inflammation and generation of oxidative stress in the vasculature. 18) Thus, the antiinflammatory and antioxidant activities of flavonoids might bring benefit for hyperuricemia and its complications. In addition, the flavonoids have increasingly aroused interest recently for their hypouricemic action in hyperuricemic animal models. [19][20][21] In the present study, we have explored hypouricemic actions from 15 flavonoids including quercetin, morin, myricetin, kaempferol, icariin, apigenin, luteolin, baicalin, silibinin, naringenin, formonoetin, genistein, puerarin, daidzin and naringin dihydrochalcone in a hyperuricemic animal model induced by potassium oxonate. We have also studied the effects of six most active compounds on serum and liver uric acid levels in normal mice. The effects on liver XOD activities were further examined in animals. MATERIALS AND METHODSMaterials Quercetin, morin, myricetin, kaempferol, icariin, apigenin, luteolin, baicalin, silibinin, naringenin, formonoetin, genistein, puerarin, daidzin and naringin dihydrochalcone were obtained commerci...

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“…The activity of hepatic xanthine oxidase (XOD) was assayed by monitoring uric acid formation at 530 nm (Sugawara et al 1999) and was expressed as nmol mg -1 protein. According to the protocol of kit (Jian Cheng Biology Company, Nanjing, China), the activities of hepatic total NOS (T-NOS) were detected.…”

Section: Biochemical Analysismentioning

confidence: 99%

Effect of trichlorfon on oxidative stress and hepatocyte apoptosis of Carassius auratus gibelio in vivo

Liu

et al. 2011

Fish Physiol Biochem

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To investigate the effect of trichlorfon on oxidative stress and hepatocyte apoptosis of Carassius auratus gibelio in vivo, the fish were exposed to 0, 0.5, 1.0, 2.0 and 4.0 mg l(-1) trichlorfon concentrations for 30 days. At the end of the experiment, plasm antioxidant activities, hepatic total nitric oxide synthase (T-NOS) activity, xanthine oxidase (XOD) activity and hepatocyte apoptosis rate were analyzed. The results showed hepatic T-NOS activities, XOD activities and hepatocyte apoptosis rate were increased with trichlorfon concentration increase. The hepatic MDA content was increased significantly at 4.0 mg l(-1) trichlorfon treatment. The disturbance of antioxidative balance was observed based on the monitoring of the plasm superoxide dismutase (SOD), catalase (CAT) activities and vitamin E levels. The current study revealed that trichlorfon influenced fish plasma antioxidative status, caused lipid peroxidation (LPO) then resulted in hepatocytes apoptosis.

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Iron depletion prevents adenine nucleotide decomposition and an increase of xanthine oxidase activity in the liver of the Long Evans Cinnamon (LEC) rat, an animal model of Wilson's disease

Cited by 18 publications

References 19 publications

Copper-induced ferroportin-1 expression in J774 macrophages is associated with increased iron efflux

Copper-induced ferroportin-1 expression in J774 macrophages is associated with increased iron efflux

Hypouricemic Action of Selected Flavonoids in Mice: Structure-Activity Relationships

Effect of trichlorfon on oxidative stress and hepatocyte apoptosis of Carassius auratus gibelio in vivo

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