Cu,Zn-SOD deficiency induces the accumulation of hepatic collagen

Sakiyama, Haruhiko; Fujiwara, Noriko; Yoneoka, Yuka; Yoshihara, Daisaku; Eguchi, Hironobu; Suzuki, Keiichiro

doi:10.3109/10715762.2016.1164856

Cited by 26 publications

(24 citation statements)

References 53 publications

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“…This assertion is supported by the observation of Kupffer cell iron deposits in NAFLD patients with enhanced apoptosis , reminiscent of the iron deposits reported in Kupffer cells of the Ctr1 int/int mouse . Loss of CuZnSOD and hepatic fibrosis were recently linked in the CuZnSOD mouse with observations of extensive collagen deposition and liver histology characterized by extensive advanced glycation end products (AGEs), which would inhibit collagen degradation . This observation supports the hypothesis that CuD may have a role in hepatic fibrosis in addition to promotion of lipogenesis.…”

Section: Copper Deficiency and Dietary Fructose Are Linked In Processsupporting

confidence: 61%

The role of insufficient copper in lipid synthesis and fatty‐liver disease

et al. 2017

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Summary The essential transition metal copper is important in lipid metabolism, redox balance, iron mobilization and many other critical processes in eukaryotic organisms. Genetic diseases where copper homeostasis is disrupted, including Menkes Disease and Wilson Disease, indicate the importance of copper balance to human health. The severe consequences of insufficient copper supply are illustrated by Menkes Disease, caused by mutation in the X-linked ATP7A gene encoding a protein that transports copper from intestinal epithelia into the bloodstream and across the blood-brain barrier. Inadequate copper supply to the body due to poor diet quality or malabsorption can disrupt several molecular level pathways and processes. Though much of the copper distribution machinery has been described and consequences of disrupted copper handling have been characterized in human disease as well as animal models, physiological consequences of sub-optimal copper due to poor nutrition or malabsorption have not been extensively studied. Recent work indicates that insufficient copper may be important in a number of common diseases including obesity, ischemic heart disease, and metabolic syndrome. Specifically, marginal copper deficiency (CuD) in has been reported as a potential etiologic factor in diseases characterized by disrupted lipid metabolism such as non-alcoholic fatty-liver disease (NAFLD). In this review, we discuss the available data suggesting that a significant portion of the North American population may consume insufficient copper, the potential mechanisms by which CuD may promote lipid biosynthesis, and the interaction between CuD and dietary fructose in the etiology of NAFLD.

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Section: Copper Deficiency and Dietary Fructose Are Linked In Processsupporting

confidence: 61%

The role of insufficient copper in lipid synthesis and fatty‐liver disease

et al. 2017

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“…In addition, Lactobacillus casei Zhang treatment also increased the hepatic levels of SOD in d-galactosamine-treated rats (Wang et al, 2013). Endogenous antioxidants, such as SOD, GSH-Px, and other antioxidant enzymes (catalase, glutathione S-transferases), reduced overgenerated ROS and free radicals (Sakiyama et al, 2016); however, LPSP-YBJ01 did not change serum GSH-Px in oxidation mice. In addition, LPSP-YBJ01 strain treatment significantly reduced serum MDA in oxidation mice, which is a biomarker of membrane lipid oxidation (Sarniak et al, 2016).…”

Section: Discussionmentioning

confidence: 91%

Lactobacillus paracasei ssp. paracasei YBJ01 reduced d-galactose–induced oxidation in male Kuming mice

Suo

Liu

et al. 2018

Journal of Dairy Science

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We investigated in vitro and in vivo antioxidant activity of Lactobacillus paracasei ssp. paracasei YBJ01 (LPSP-YBJ01) isolated and identified from fermented yogurt. Strain LPSP-YBJ01 had stress tolerance against acidity, bile salt, and osmotic pressure. Five in vitro antioxidant assays were used to evaluate antioxidant activity of LPSP-YBJ01, which could scavenge free radicals (2,2-diphenyl-1-picrylhydrazyl and hydroxyl) and superoxide anion in vitro. In addition, strain LP-SP-YBJ01 had stronger antilipid peroxidation activity and weak reducing power in vitro. We measured in vivo antioxidant activity of LPSP-YBJ01 in an oxidation mouse model induced by d-galactose injection. Strain LPSP-YBJ01 significantly increased serum superoxide dismutase (SOD), glutathione peroxidase, and total-antioxidant capability, and inhibited generation of malondialdehyde in a dose-dependent manner. In addition, strain LPSP-YBJ01 also increased the hepatic and splenic protein expressions of some antioxidant enzymes such as catalase, Cu/Zn-SOD, and Mn-SOD in mice treated with d-galactose. Thus, LPSP-YBJ01 had antioxidant activity in vitro and in vivo and may be a useful probiotic.

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“…On the other hand, SOD1 is known to be an ALS-causative protein, and the aggregation of mutant SOD1 is a pathological hallmark in familial forms of ALS with mutations in the SOD1 gene [ 14 – 16 ]. Although SOD1 knockout mice show some impairments [ 17 , 18 ], they do not develop ALS-like symptoms [ 19 ]. SOD1 is a homodimer containing one copper ion required for enzymatic activity and one zinc ion required for the protein stability in each 16-kDa subunit.…”

Section: Introductionmentioning

confidence: 99%

Cu/Zn-superoxide dismutase forms fibrillar hydrogels in a pH-dependent manner via a water-rich extended intermediate state

et al. 2018

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Under certain conditions, amyloid-like fibrils can develop into three-dimensional networks and form hydrogels by a self-assembly process. When Cu/Zn superoxide dismutase (SOD1), an anti-oxidative enzyme, undergoes misfolding, fibrillar aggregates are formed, which are a hallmark of a certain form of familial amyotrophic lateral sclerosis (ALS). However, the issue of whether SOD1 fibrils can be assembled into hydrogels remains to be tested. Here, we show that the SOD1 polypeptides undergo hydrogelation accompanied by the formation of thioflavin T-positive fibrils at pH 3.0 and 4.0, but not at pH 5.0 where precipitates are formed. The results of viscoelastic analyses indicate that the properties of SOD1 hydrogels (2%) were similar to and slightly more fragile than a 0.25% agarose gel. In addition, monitoring by a quartz crystal microbalance with admittance analysis showed that the denaturing of immobilized SOD1 on a sensor under the hydrogelation conditions at pH 3.0 and 4.0 resulted in an increase in the effective acoustic thickness from ~3.3 nm (a folded rigid form) to ~50 and ~100 nm (an extended water-rich state), respectively. In contrast, when SOD1 was denatured under the same conditions at pH 5.0, a compact water-poor state with an effective acoustic thickness of ~10 nm was formed. The addition of physiological concentrations of NaCl to the pH 4.0 sample induced a further extension of the SOD1 with larger amounts of water molecules (with an effective acoustic thickness of ~200 nm) but suppressed hydrogel formation. These results suggest that different denatured intermediate states of the protein before self-assembly play a major role in determining the characteristics of the resulting aggregates and that a conformational change to a suitable level of extended water-rich intermediate state before and/or during intermolecular assembling is required for fibrillation and hydrogelation in the case of globular proteins.

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Cu,Zn-SOD deficiency induces the accumulation of hepatic collagen

Cited by 26 publications

References 53 publications

The role of insufficient copper in lipid synthesis and fatty‐liver disease

The role of insufficient copper in lipid synthesis and fatty‐liver disease

Lactobacillus paracasei ssp. paracasei YBJ01 reduced d-galactose–induced oxidation in male Kuming mice

Cu/Zn-superoxide dismutase forms fibrillar hydrogels in a pH-dependent manner via a water-rich extended intermediate state

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