Ultrastructural studies of vascular and muscular changes in ascorbic acid deficient guinea-pigs

Kim, J. C. S.

doi:10.1258/002367777781005433

Cited by 6 publications

(4 citation statements)

References 5 publications

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“…As such, Lepr db/+ Smp30 Y/− and Lepr db/db Smp30 Y/− mice were given vitamin C-supplemented water in this study. Vitamin C is known to play an important role in the structure and function of mitochondria and endoplasmic reticulum [33]. Harrison et al reported that vitamin E and vitamin C treatment improves fibrosis but not necroinflammation in NASH patients [34].…”

Section: Discussionmentioning

confidence: 99%

Leprdb/db Mice with Senescence Marker Protein-30 Knockout (Leprdb/dbSmp30Y/−) Exhibit Increases in Small Dense-LDL and Severe Fatty Liver Despite Being Fed a Standard Diet

et al. 2013

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Background/AimsThe senescence marker protein-30 (SMP30) is a 34 kDa protein originally identified in rat liver that shows decreased levels with age. Several functional studies using SMP30 knockout (Smp30Y/−) mice established that SMP30 functions as an antioxidant and protects against apoptosis. To address the potential role of SMP30 in nonalcoholic fatty liver disease (NAFLD) pathogenesis, we established Smp30Y/− mice on a Leprdb/db background (Leprdb/dbSmp30Y/− mice).Research Design/Principal FindingsMale Leprdb/dbSmp30Y/− mice were fed a standard diet (340 kcal/100 g, fat 5.6%) for 16 weeks whereupon the lipid/lipoprotein profiles, hepatic expression of genes related to lipid metabolism and endoplasmic reticulum stress markers were analyzed by HPLC, quantitative RT-PCR and western blotting, respectively. Changes in the liver at a histological level were also investigated. The amount of SMP30 mRNA and protein in livers was decreased in Leprdb/dbSmp30Y/+ mice compared with Leprdb/+Smp30Y/+ mice. Compared with Leprdb/dbSmp30Y/+ mice, 24 week old Leprdb/dbSmp30Y/− mice showed: i) increased small dense LDL-cho and decreased HDL-cho levels; ii) fatty liver accompanied by numerous inflammatory cells and increased oxidative stress; iii) decreased mRNA expression of genes involved in fatty acid oxidation (PPARα) and lipoprotein uptake (LDLR and VLDLR) but increased CD36 levels; and iv) increased endoplasmic reticulum stress.ConclusionOur data strongly suggest that SMP30 is closely associated with NAFLD pathogenesis, and might be a possible therapeutic target for NAFLD.

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Section: Discussionmentioning

confidence: 99%

Leprdb/db Mice with Senescence Marker Protein-30 Knockout (Leprdb/dbSmp30Y/−) Exhibit Increases in Small Dense-LDL and Severe Fatty Liver Despite Being Fed a Standard Diet

et al. 2013

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“…Myofilaments are fragmented and mitochondria swollen (Kim, 1977). Epiphyseal growth centers of long bones are deranged with greatly reduced osteoid formation, degenerating and deranged chondrocytes, decreased bony trabeculae in the marrow cavity, reduced osteoclastic and increased osteoblastic activity, and multiple microfractures.…”

Section: Hypovitaminosis Cmentioning

confidence: 99%

“…A history of inappropriate feed, decreased prothrombin time, and a serum vitamin C level below 0.55 mg/dl (normal around 2.01 mg/dl) indicate hypovitaminosis C (Kim, 1977). A history of inappropriate feed, decreased prothrombin time, and a serum vitamin C level below 0.55 mg/dl (normal around 2.01 mg/dl) indicate hypovitaminosis C (Kim, 1977).…”

Section: Hypovitaminosis Cmentioning

confidence: 99%

Biology and Diseases of Guinea Pigs

Shomer

Holcombe

Harkness

2015

Laboratory Animal Medicine

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“…That is the main reason why guinea pig is widely used laboratory model for examining of the oxidative stress (9)(10)(11). The inability to produce endogenous ascorbic acid makes results from guinea pigs extrapolatable to humans (12)(13)(14). Except the inability to synthesize vitamin C there are other similarities like a similar response of lipid metabolism to dietary intervention (15).…”

Section: Introductionmentioning

confidence: 99%

Effect of Intramuscular Injection on Oxidative Homeostasis in Laboratory Guinea Pig Model

Kracmarova

Banďouchová

Pikula

et al. 2016

Acta Med. (Hradec Kralove, Czech Repub.)

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In animal models, there was observed alteration of various physiological processes caused by microtraumas. Here reported experiment was aimed on the research of link between injection and development of an oxidative imbalance. Laboratory guinea pig was chosen as a suitable model for examining of the oxidative stress. Markers indicating oxidative homeostasis were assayed in the frontal, temporal and occipital brain lobe, cerebellum, liver, kidney, spleen and heart one hour after an intramuscular injection. Common biochemical parameters were measured in plasma samples as well. The most extensive effect was observed in the heart where the thiobarbituric acid reactive substances value was more than twice increased after the injection. The level of carbonylated proteins was significantly elevated in the kidney and ferric reducing antioxidant power value was increased in the brain compartments. The enzyme activities in the organs were not influenced except the activity of superoxide dismutase, which was moderately decreased in the brain. In the plasma samples, there was observed increase of the blood urea nitrogen. The results showed significant the influence of the intramuscular injection on a development of an oxidative insult. The injection can be considered as an adverse effect with quite extensive stress consequences.

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Ultrastructural studies of vascular and muscular changes in ascorbic acid deficient guinea-pigs

Cited by 6 publications

References 5 publications

Leprdb/db Mice with Senescence Marker Protein-30 Knockout (Leprdb/dbSmp30Y/−) Exhibit Increases in Small Dense-LDL and Severe Fatty Liver Despite Being Fed a Standard Diet

Leprdb/db Mice with Senescence Marker Protein-30 Knockout (Leprdb/dbSmp30Y/−) Exhibit Increases in Small Dense-LDL and Severe Fatty Liver Despite Being Fed a Standard Diet

Biology and Diseases of Guinea Pigs

Effect of Intramuscular Injection on Oxidative Homeostasis in Laboratory Guinea Pig Model

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