• Toxicological Research
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• v.28 no.3
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• pp.179-185
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• 2012

Paecilomyces sinclairiis (PS) is known as a functional food or human health supplement. However concerns have been raised about its kidney toxicity. This study was performed to investigate the kidney toxicity of PS by 13 week-oral administration to rats. Blood urea nitrogen (BUN), serum creatinine, and kidney damage biomarkers including beta-2-microglobulin (${\beta}2m$), glutathione S-transferase alpha (GST-${\alpha}$), kidney injury molecule 1 (KIM-1), tissue inhibitor of matrix metalloproteinase 1 (TIMP-1), vascular endothelial growth factor (VEGF), calbindin, clusterin, cystatin C, neutrophil gelatinase-associated lipocalin (NGAL) and osteopontin were measured during or after the treatment of PS. BUN, creatinine and kidney damage biomarkers in serum were not changed by PS. However, kidney cell karyomegaly and tubular hypertrophy were observed dose-dependently with higher severity in males. KIM-1, TIMP-1 and osteopontin in kidney and urine were increased dose dependently in male or at the highest dose in female rats. Increased urinary osteopontin by PS was not recovered at 2 weeks of post-exposure in both genders. Cystatin C in kidney was decreased at all treatment groups but inversely increased in urine. The changes in kidney damage biomarkers were more remarkable in male than female rats. These data indicate that the PS may provoke renal cell damage and glomerular filtration dysfunction in rats with histopathological lesions and change of kidney damage biomarkers in kidney or urine. Kidney and urinary KIM-1 and cystatin C were the most marked indicators, while kidney weight, BUN and creatinine and kidney damage biomarkers in serum were not influenced.

• Applied Microscopy
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• v.17 no.1
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• pp.115-130
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• 1987

The present experiment was performed to investigate the acute effects of cadmium on ultrastructural and biochemical changes in mouse kidney and compare these changes with liver damage. Mouse were injected with cadmium chloride at a dose of 5 mg/kg body weight. After treatment, mouse were sacrificed at time intervals of 6, 12, 24 and 48 hours. It was observed that ultrastructural changes in mouse kidney were composed of swelling of mitochondria, dilation in endoplasmic reticulum, wrinkling at basal infolded membrane, formation of autophagosome and partial loss of microvilli in brush. border, and that ultrastructural changes in liver were mitochondrial change, dilation and deterioration of rough endoplasmic reticulum and proliferation of smooth endoplasmic reticulum. Biochemical effects of cadmium were more severe on liver than kidney. Therefore, acutely injected cadmium caused not only liver damage, but also kidney damage.

• The Korean Journal of Physiology and Pharmacology
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• v.27 no.3
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• pp.257-265
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• 2023

Kidney ischemia/reperfusion (I/R) injury, a common cause of acute kidney injury (AKI), is associated with the migration of inflammatory cells into the kidney. Ras-related C3 botulinum toxin substrate 1 (Rac1), a member of the Rho family of small GTPase, plays an important role in inflammatory cell migration by cytoskeleton rearrangement. Here, we investigated the role of Rac1 on kidney I/R injury and macrophage migration. Male mice were subjected to either 25 min of bilateral ischemia followed by reperfusion (I/R) or a sham operation. Some mice were administrated with either NSC23766, an inhibitor of Rac1, or 0.9% NaCl (vehicle). Kidney damage and Rac1 activity and expression were measured. The migration and lamellipodia formation of RAW264.7 cells, mouse monocyte/macrophage, induced by monocyte chemoattractant protein-1 (MCP-1, a chemokine) were determined using transwell migration assay and phalloidin staining, respectively. In sham-operated kidneys, Rac1 was expressed in tubular cells and interstitial cells. In I/R-injured kidneys, Rac1 expression was decreased in tubule cells in correlation with the damage of tubular cells, whereas Rac1 expression increased in the interstitium in correlation with an increased population of F4/80 cells, monocytes/macrophages. I/R increased Rac1 activity without changing total Rac1 expression in the whole kidney lysates. NSC23766 administration blocked Rac1 activation and protected the kidney against I/R-induced kidney damage and interstitial F4/80 cell increase. NSC23766 suppressed monocyte MCP-1-induced lamellipodia and filopodia formation and migration of RAW 264.7 cells. These results indicate Rac1 inhibition protects the kidney against I/R via inhibition of monocytes/macrophages migration into the kidney.

• Journal of Marine Bioscience and Biotechnology
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• v.13 no.2
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• pp.86-93
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• 2021

A high salt diet contributes to kidney damage by causing hypoxia and oxidative stress. Recently, an increase in dietary salt has been reported to induce an inflammatory phenotype in immune cells, further contributing to kidney damage. However, studies on the exact mechanism and role of a high salt diet on the inflammatory response in the kidneys are still insufficient. In this study, a cisplatin-induced acute kidney injury model using C57BL/6 mice was used to analyze the effect of salt intake on kidney injury. Results showed that high salt administration aggravated kidney edema in mice induced by treatment with cisplatin. Moreover, the indicators of kidney and liver function impairment were significantly increased in the group cotreated with high salt compared with that treated with cisplatin alone. Furthermore, the exacerbation of kidney damage by high salt administration was also associated with a decrease in the number of cells in the immune regulatory system. Additionally, high salt administration further decreased renal perfusion functions along with increased cisplatin-induced damage to proximal tubules. This was accompanied by increased expression of T cell immunoglobulin, mucin domain 1 (a biomarker of kidney injury), and Bax (a pro-apoptotic factor). Moreover, cisplatin-induced expression of proinflammatory mediators and cytokines, including cyclooxygenase-2 and tumor necrosis factor-α in kidney tissue, was further increased by high salt intake. Therefore, these results indicate that the kidney's inflammatory response by high salt treatment can further promote kidney damage caused by various pathological factors.

• The Journal of the Korea Contents Association
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• v.9 no.12
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• pp.376-384
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• 2009

This research has microstructure observation to find tissue damage mechanism and radio-protection effect on mouse kidney tissue. The result observation of a Light Microscope(LM); The kidney tissue after 5Gy irradiation observed a glomerulus atrophy, also crack distance to base membrane of a convoluted tubules. The kidney tissue after 10Gy irradiation observed out flow cytoplasm to membrane break of a convoluted tubules. The result observation of a Transmission Electron Microscope(TEM); The kidney tissue of after 5Gy irradiation has to breaking a inside cristae and membrane of mitochondria, also show definite damage of nucleus membrane. 10Gy irradiation has all the more damage a base membrane and thickness of lysosome. However, Propolis eating groups observed normal to nucleus membrane and small body of intracellular. therefore We considered "Propolis" as make radio protection function to kidney tissue of the greater part.

• Journal of radiological science and technology
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• v.43 no.1
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• pp.29-34
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• 2020

Mitochondria was observed much around the nuclear membrane of liver tissue where the energy metabolism process is active. Testis tissue had a large number of undifferentiated cells, and cristae in Inner membrane of Mitochondria was not observed clearly. Morphological damage occurred first in Inner membrane rather than the outer membrane. The kidney tissue was clearly observed in the form of cristae. Radiation-induced damage occurred at the edges of both ends, and the membrane was observed bursting with the thickness of the outer membrane. Small intestine cells were observed in many mitochondria in the tissues around the villus, where bowel movements were active. Morphological damage occurred with the outer and inner membranes getting tangled. Mitochondria sensitivity to radiation was sensitized in testis and small intestine tissues, and kidney, ovary and liver tissues were found to be resistant.

• Journal of the Korean Society of Food Science and Nutrition
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• v.28 no.2
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• pp.471-476
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• 1999

The effects of total dietary restriction(100% restriction of energy intake) on thiobarbituric acid reactive substance(TBARS) contents and intracellular antioxidant enzymes activities in the liver and kidney of young male Sprague Dawley rats were studied. The TBARS contents were reduced in both liver and kidney, up to 77% and 79% of the control rats, fed ad libitum, respectively at 7 days after dietary restriction . Superoxide dismutase(SOD) activities in the liver and kidney of rats were increased significantly by total dietary restriction. However, the activity of catalase in kidney was decreased 27% at 6 days after dietary restriction, but this enzyme activity did not change in liver. The changes of glutathione peroxidae(GSHPx) and catalase activities in the liver and kidney of rats with dietary restriction were not significant. These result suggested that dietary restriction reduce the free radical induced by tissue damage, as determined by TBARS content, in both the liver and kidney but the changes of activities of antioxidant enzymes may not be a contributory factor in reducing oxidative damage to tissue.

• Biomolecules & Therapeutics
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• v.20 no.3
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• pp.268-272
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• 2012

Nephrotoxicity occurs when kidney-specific detoxification and excretion do not work properly due to the damage or destruction of kidney function by exogenous or endogenous toxicants. Exposure to drugs often results in toxicity in kidney which represents the major control system maintaining homeostasis of body and thus is especially susceptible to xenobiotics. Understanding the toxic mechanisms for nephrotoxicity provides useful information on the development of drugs with therapeutic benefits with reduced side effects. Mechanisms for drug-induced nephrotoxicity include changes in glomerular hemodynamics, tubular cell toxicity, inflammation, crystal nephropathy, rhabdomyolysis, and thrombotic microangiopathy. Biomarkers have been identified for the assessment of nephrotoxicity. The discovery and development of novel biomarkers that can diagnose kidney damage earlier and more accurately are needed for effective prevention of drug-induced nephrotoxicity. Although some of them fail to confer specificity and sensitivity, several promising candidates of biomarkers were recently proved for assessment of nephrotoxicity. In this review, we summarize mechanisms of drug-induced nephrotoxicity and present the list of drugs that cause nephrotoxicity and biomarkers that can be used for early assessment of nephrotoxicity.

• The Journal of Internal Korean Medicine
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• v.26 no.4
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• pp.767-775
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• 2005

This study was carried out to investigate the preventive effect of Salviae Miltiorrhizae Radix, Rhei Rhizoma and Carthami Flos combined with Samgijiwhang-Tang(SJTSRC) on streptozotocin(STZ)-induced diabetic nephropathy. Rats were divided into a control group of rats with STZ-induced diabetic nephropathy, a sample group of those given SJTSRC, and a normal group. In the experiment diabetic nephropathy was induced by giving STZ(60mg/kg) to rats via the peritoneum, and effects were assessed with measures of serum creatinine, serum BUN, secretion content of albumin and glucose content of urine, malondialdehyde(MDA) and glutathione(GSH) content in cortex of kidney. When STZ was injected into sample rat, the value of creatinine and BUN increased validly and STZ did damage to the kidney. When applying SJTSRC to sample rats, the value of serum creatinine decreased validly but the value of serum BUN decreased invalidity. It was confirmed that SJTSRC had an effect on recovery after kidney damage and secretion content of albumin increasedafter administration of SJTSRC but there was no change in glucose content of urine compared with the control group. The decrease of secretion of albumin after injection of STZ was taken to mean progressive diabetic nephropathy, and that reversal of that trend after SJTSRC administration showed that kidney function had improved, not through decreasing blood sugar, but through other factors. Results suggest that diabetic nephropathy was induced by STZ, and SJTSRC was effective in restricting the extent of damage to the kidney and halting the progression of diabetic nephropathy with improvement in levels of serum creatinine and albumin secretion. More study is needed, particularity pertaining to anti-oxidative effects in the kidney cortex.

• BMB Reports
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• v.45 no.11
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• pp.671-676
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• 2012

Caloric restriction (CR) has been associated with health benefits and these effects have been attributed, in part, to modulation of oxidative status by CR; however, data are still controversial. Here, we investigate the effects of seventeen weeks of chronic CR on parameters of oxidative damage/modification of proteins and on antioxidant enzyme activities in cardiac and kidney tissues. Our results demonstrate that CR induced an increase in protein carbonylation in the heart without changing the content of sulfhydryl groups or the activities of superoxide dismutase and catalase (CAT). Moreover, CR caused an increase in CAT activity in kidney, without changing other parameters. Protein carbonylation has been associated with oxidative damage and functional impairment; however, we cannot exclude the possibility that, under our conditions, this alteration indicates a different functional meaning in the heart tissue. In addition, we reinforce the idea that CR can increase CAT activity in the kidney. Moreover, CR caused an increase in CAT activity in kidney, without changing other parameters. Protein carbonylation has been associated with oxidative damage and functional impairment; however, we cannot exclude the possibility that, under our conditions, this alteration indicates a different functional meaning in the heart tissue. In addition, we reinforce the idea that CR can increase CAT activity in the kidney.