• Korean Journal of Animal Reproduction
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• v.25 no.1
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• pp.43-49
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• 2001

This study was performed to elucidate the effects of copper poisoning on the reproductive organ of rats. After consecutive oral administrations of copper sulfate, the weights of testis, the numbers and motilities of sperms, organ weights and histological changes of testes were compared between control and experimental groups. 1. Testis weights of 1,000, 2,000 or 4,000 ppm/kg of copper sulfate-administrated rats gradually decreased compared with control group, and the values no significant changes. 2. The sperm numbers of 1,000, 2,000 or 4,000 ppm/kg of copper sulfate-administrated rats were lowered in dose dependent manners than those of control group's and the values no significant changes. 3, The motilities sperms of 1,000, 2,000 or 4:000 ppm/kg of copper sulfate-administrated rats decreased significantly in dose-dependent manners compared with those of control group's. 4. The weights of livers and kidneys of 1,000, 2,000 or 4,000 ppm/kg of copper sulfate-administration rats decreased or increased. 5. Necrosis of hepatocytes around the central veins and infiltrations of fine granules-harboring macrophages in periportal and interstitial tissues were found out in the livers of copper sulfate-administrated rats. The Bowman's capsule and tubules of kidneys were filled with hyaline material.

• Childhood Kidney Diseases
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• v.14 no.2
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• pp.132-142
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• 2010

Hypokalemia usually reflects total body potassium deficiency, but less commonly results from transcellular potassium redistribution with normal body potassium stores. The differential diagnosis of hypokalemia includes pseudohypokalemia, cellular potassium redistribution, inadequate potassium intake, excessive cutaneous or gastrointestinal potassium loss, and renal potassium wasting. To discriminate excessive renal from extrarenal potassium losses as a cause for hypokalemia, urine potassium concentration or TTKG should be measured. Decreased values are indicative of extrarenal losses or inadequate intake. In contrast, excessive renal potassium losses are expected with increased values. Renal potassium wasting with normal or low blood pressure suggests hypokalemia associated with acidosis, vomiting, tubular disorders or increased renal potassium secretion. In hypokalemia associated with hypertension, plasam renin and aldosterone should be measured to differentiated among hyperreninemic hyperaldosteronism, primary hyperaldosteronism, and mineralocorticoid excess other than aldosterone or target organ activation. Hypokalemia may manifest as weakness, seizure, myalgia, rhabdomyolysis, constipation, ileus, arrhythmia, paresthesias, etc. Therapy for hypokalemia consists of treatment of underlying disease and potassium supplementation. The evaluation of hyperkalemia is also a multistep process. The differential diagnosis of hyperkalemia includes pseudohypokalemia, redistribution, and true hyperkalemia. True hyperkalemia associated with decreased glomerular filtration rate is associated with renal failure or increased body potassium contents. When glomerular filtration rate is above 15 mL/min/$1.73m^2$, plasma renin and aldosterone must be measured to differentiate hyporeninemic hypoaldosteronism, primary aldosteronism, disturbance of aldosterone action or target organ dysfunction. Hyperkalemia can cause arrhythmia, paresthesias, fatigue, etc. Therapy for hyperkalemia consists of administration of calcium gluconate, insulin, beta2 agonist, bicarbonate, furosemide, resin and dialysis. Potassium intake must be restricted and associated drugs should be withdrawn.

• Childhood Kidney Diseases
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• v.8 no.2
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• pp.149-158
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• 2004

Purpose : In order to evaluate the value of the renal expression of ICAM-1 as a marker of renal injury, we analyzed the relationship between abnormal tubular expression of ICAM-1 and histopathological features and clinical manifestations in children with IgA nephropathy (IgAN). Methods: The clinical data from 43 patients with IgAN were analyzed retrospectively and compared to the histopathologic subclassification proposed by Haas. ICAM-1 in tubular epithelium was assessed using the LSAB(Labeled streptavidine biotin) kit on the renal biopsy specimens. Results: In 43 patients with primary IgAN, 28 males and 15 females aged $12.2{\pm}2.2$ years were studied. There were no differences of renal tubular expression of ICAM-1 between patients with gross hematuria and without gross hematuria. But renal tubular expression of ICAM-1 in patients with proteinuria was significantly higher than that of in patients without proteinuria($78.2{\pm}14.19%\;vs\;55.8{\pm}32.20%,\;P<0.05$). Renal tubular expression of ICAM-1 was also associated with the severity of histopathological degree using Haas classification method. In subclass I, renal tubular expression of ICAM-1 was significantly lower than those of other subclasses. A significant correlation was found between the tubular expression of ICAM-1 and the total amount of protein in 24 hour collected urine$(r_s=0.47236,\;p<0.05)$. But there were no significant correlations between the renal tubular expression of ICAM-1 and interstitial cellular infiltration, tubular atrophy, and interstitial fibrosis respectively(F=0.89, P>0.05; F=0.31, p>0.05; F=0.21, p>0.05). Conclusion: Renal tubular expression of ICAM-1 can be a useful marker of renal injury in children with IgAN. (J Korean Soc Pediatr Nephrol 2004;8:149-158)

• Clinical and Experimental Pediatrics
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• v.52 no.1
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• pp.119-123
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• 2009

Renal cell carcinoma (RCC) arising from epithelial cells of the renal tubules is a highly aggressive and malignant tumor in all ages; however, it rarely occurs in children. the standard treatment for RCC is radical nephrectomy with lymph node dissection when the tumor is localized and can be completely resected. Adjuvant chemotherapy, radiotherapy, and immunotherapy are used for pediatric patients with advanced RCC involving lymph nodes or metastatic lesions. Sorafenib is an oral, multikinase inhibitor that has recently been approved for use in metastatic RCC. Common toxicities that have been reported include dermatologic changes such as rash or desquamation and hand-foot skin reaction, diarrhea, fatigue, alopecia, and hypertension. In particular, hand-foot syndrome (HFS) an erythematous skin lesion of the palms and solesis most often caused by cytostatic chemotherapeutic agents. In this report, we have studied a 14-year-old female patient with hand-foot syndrome that occurred in association with sorafenib for the treatment of metastatic RCC. Furthermore, this case demonstrates that reversal of complications can be achieved by discontinuing the drug and intervention with topical steroids, vitamin E, and high-dose pyridoxine.

• Journal of Food Hygiene and Safety
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• v.8 no.1
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• pp.37-53
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• 1993

F. moniliforme MRC 826, a common fungal contaminant of com, has been known to produce a group of mycotoxins, the fumonisins. By thin layer chromatography, fumonisin $B_{1}$ was detected in the F. moniliforme MRC 826 com culture material(CM) extracts. This study was performed to compare the toxicity and carcinogenicity of F. moniliforme MRC 826 CM with those of aflatoxin $B_1(AFB_1)$ in rats. The toxicity was tested over a period of 7 days in ten female Sprague-Dawley (SD) rats. Treatment group were fed a 1 : 1 mixture(wt/wt) of ground CM and basal diet in powder form, while other negative control group were given basal diet alone. The principal pathological changes in rats treated with 50% CM were hepatocellular hydropic degeneration and renal tubular necrosis. The cancer-promoting activity of CM was evaluated in the rat liver diethylnitrosamine-two thirds partial hepatectomy(DEN-PH) model for carcinogenesis. 70 male SO rats(ca. 170 g) were randomized into 5 groups. Group I served as the positive controls and received the basal diet containing 2 ppm $AFB_{1}$ group 2 received 5% CM, group 3 received 2.5% CM, group 4 received 5% normal com and group 5 received 2.5% normal com. 5% treated group showed cancer promoting activity in rat liver using DEN as initiator and the induction of glutathione S-transferase placental form positive foci as an end point after 6 weeks of promotion.

• Applied Biological Chemistry
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• v.8
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• pp.101-111
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• 1967

Daily doses of phenylmercuric acetate arranged in $30{\gamma}\;(group\;I)$, 3{\gamma}\;(group\;II)$ and $0.3{\gamma}\;(group\;III)$ were administered respectively to rabbits for 90 days. The chief histopathological changes in the organs and the analytical data on mercury residues in the excretion and liver were as follows. 1. Kidney: In group I, severe degrees of vacuolization and cloudy swelling were occurred in the epithelial cells of proximal convoluted tubules and severe cloudy swelling and coagulative necrosis were observed in the proximal straight tubules. There were many hyaline casts in the collecting tubules. In group II, moderate degrees of vacuolization and cloudy swelling were observed in the epithelial cells of proximal convoluted tubules and moderate cloudy swelling and coagulative necrosis were encountered in the proximal straight tubules. A little numbers of hyaline casts were located in the lumen of collecting tubules. In group III, slight degree of cloudy swelling were observed in the epithelial cells of proximal convoluted and straight tubules. 2. Liver: In group I, cloudy swelling, fatty changes and coagulative necrosis were observed in the central zone of hepatic lobules. Dissociation of hepatic cell cords was encountered. Hyperplsia of hepatic cells were remarkable in group II. No Pathological changes were observed in group III. 3. Spleen: Deposition of hemosiderin pigment was prominant in group I and small amount of the pigment was observed in group II. There were no pathological changes in group III. 4. Adrenal, colon and heart: No pathological changes were detected in all 3 groups. 5. In an average about 76.5% of mercury was excreted from group I, 85.4% from group II and 79.8% from group III. 6. Mercury content in the liver was 0.0348 g in group I, 0.00378 g and 0.00066 g in group II and group III respectively. 7. In general, as to increased mercury doses the concentration of mercury accumulation in the liver became higher, how·ever, the accumulation quantity against a total amount of mercury doses showed an adverse trend. In other word, the quantity of mercury accumulation was not increased proportionately by higher dose of mercury.

• Korean Journal of Veterinary Research
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• v.37 no.2
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• pp.311-319
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• 1997

The mechanisms of $estradiol-17{\beta}$ regulating growth of both normal and neoplastic cells are not clear until now. In studies using various estrogen-dependent breast cell lines, it is recently known that estrogen controls the cell growth by regulating the expression of growth factors and/or their receptors. In the present study, we investigated the effects of $estradiol-17{\beta}$on cell growth and IGF-I binding sites using primary cultured renal proximal tubule cells. We have obtained results as follows : $Estradiol-17{\beta}(10^{-9})$ has stimulatory effects in cell growth. Cotreatment of $estradiol-17{\beta}(10^{-9}M)$ and $IGF-I(5{\times}10^{-8}M)$ significantly increased the growth of primary rabbit renal proximal tubule cells compared to that of $estradiol-17{\beta}$ or IGF-I alone treated cells. In binding studies, we found that the binding of $^{125}IGF-I$ on cell membranes was incubation time- and temperature-dependent. Incubation at $37^{\circ}C$ results in higher binding of $^{125}IGF-I$ than that of $23^{\circ}C$ or $4^{\circ}C$. Maximum binding was observed at $37^{\circ}C$ between 30 and 60 minutes. The binding of $^{125}IGF-I$ to both control and $estradiol-17{\beta}-treated$ cells was inhibited by unlabelled $IGF-I(10^{-8}{\sim}10^{-12}M)$ in a concentration-dependent manner. However, EGF did not compete for $^{125}IGF-I$ binding at $10^{-8}{\sim}10^{-12}M$. IGF-I binding to the membranes from both control and $estradiol-17{\beta}-treated$ cells was also analyzed. We found that $estradiol-17{\beta}-treated$ cells exhibited higher binding activity for IGF-I. When $estradiol-17{\beta}$ or tamoxifen alone, or $estradiol-17{\beta}$ and tamoxifen cotreated cells were compared, the binding ratio of $^{125}I-IGF-I$ of $estradiol-17{\beta}-treated$ cell was significantly increased but was similar to control in both $estradiol-17{\beta}$ and tamoxifen cotreated cell. These results suggest that $estradiol-17{\beta}$ in part controls cell proliferation by regulating the expression of IGF-I receptors in primary rabbit renal proximal tubule cells.

• Korean Journal of Veterinary Research
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• v.37 no.2
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• pp.301-310
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• 1997

Diabetes mellitus is associated with a wide range of pathophysiological in the kidney. This study was designed to examine the effects of high glucose concentration on IGF-I binding and glucose transporters in renal proximal tubule cells. The results were as follows : The binding of $^{125}I-IGF-I$ reached the peak at the 30 minutes and gradually decreased by the time dependent manner. The binding of $^{125}I-IGF-I$ was inhibited by the unlabelled IGF-I($10^{-14}{\sim}10^{-8}M$) in a concentration dependent manner. The relative affinity of IGF-I receptor for IGF-I, IGF-II and insulin exhibited typical type 1 binding(IGF-I > insulin > IGF-II). However IGF-II did not compete for the cultured cell membrane $^{125}I-IGF-I$ binding site at $10^{-14}{\sim}10^{-8}M$. Under optimal conditions, IGF-I binding to the membranes from 5mM and 20mM glucose treated cells was analyzed. It was found that 20mM glucose treated cells exhibited higher binding activity for IGF-I. In order to further substantiate this increase in IGF-I binding sites, we performed affinity-labelling studies. The cross-linked cell membrane subjected to SDS-PAGE; labelled material was detected by autoradiography. 20mM glucose treated cells exhibited higher levels. The initial rate of $methyl-{\alpha}-D-glucopyranoside({\alpha}-MG)$ uptake was significantly lower($74.41{\pm}6.71%$) in monolayers treated with 20mM glucose than those of 5mM glucose. However, 3-O-methyl-D-glucose(3-O-MG) uptake was not affected by glucose concentration in culture media. IGF-I significantly increased ${\alpha}-MG$ uptake in both 5mM and 20mM glucose treated cells. However, 3-O-MG uptake was not affected by IGF-I in both conditions. In conclusion, 20mM glucose increased binding sites of $^{125}I-IGF-I$, inhibited Na/glucose cotransporter activity. But 20mM glucose did not change facilitated glucose transporter.

• Journal of Acupuncture Research
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• v.17 no.3
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• pp.208-218
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• 2000

This study was undertaken to determine if Salviae Radix (SR) exerts protective effect against oxidant-induced inhibition of phosphate uptake in renal proximal tubular cells. Membrane transport function and cell death were evaluated by measuring phosphate uptake and trypan blue exclusion, respectively, in opossum kidney (OK) cells, an established proximal tubular cell line. $H_2O_2$ was used as a model oxidant. $H_2O_2$ inhibited the phosphate uptake in a dose-dependent manner over the concentration range of 0.1-0.5 mM. Similar fashion was observed in cell death. However, the phosphate uptake was more vulnerable to $H_2O_2$ than cell death, suggesting that $H_2O_2$-induced inhibition of phosphate uptake is not totally attributed to cell death. Decreasedphosphate uptake was associated with ATP depletion and inhibition of $Na^+$-pump activity as determined by direct inhibition of $N^+-K^+$-ATPase activity. When cells were treated with $H_2O_2$ in the presence of 0.05% SR, the inhibition of phosphate uptake and cell death induced by $H_2O_2$ was significantly attenuated. SR restored ATP depletion and decreased $Na^+-K^+$-ATPase activity, and this is likely responsible for the protective effect of SR on decreased phosphate uptake. The protective effect of SR was similar to the $H_2O_2$ scavenger catalase. SR reacts directly with $H_2O_2$ to reduce the effective concentration of the oxidant. The iron chelator deferoxamine prevented the inhibition of phosphate uptake and cell death induced by $H_2O_2$, suggesting that $H_2O_2$-induced cell injury is resulted from an iron-dependent mechanism. These results indicate that SR exerts the protective effect against $H_2O_2$-induced inhibition of phosphate uptake by reacting directly with $H_2O_2$ like the $H_2O_2$scavenger enzyme catalase, in OK cells. However, the underlying mechanism remains to be explored.

• Childhood Kidney Diseases
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• v.8 no.2
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• pp.186-194
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• 2004

Purpose: Membranoproliferative glomeulonephritis(MPGN) has been diagnosed in an increasing number of asymptomatic cases. These cases have been detected by school urinary screening test even though the total cases of MPGN show a decreasing trend. We have analyzed the clinical and pathological characteristics of children with MPGN according to the clinical manifestations at the time of disease presentation. Methods: A total of 18 patients who had been diagnosed with idiopathic MPGN by percutaneous renal biopsy from January 1990 to February 2004 were involved in our study. The patients were divided into 2 groups as the school urinary screening(A) group and the symptomatic(S) group according to the clinical manifestations at the time of disease presentation. Results: Out of the total 18 patients, 8(44.4%) were in the S group and 10(55.6%) were in the A group. The mean serum total protein, albumin and $C_3$ levels in the S group were significantly lower than those levels of the A group, respectively($4.9{\pm}1.2\;g/dL,\;vs\;7.0{\pm}0.5\;g/dL\;P=0.002,\;2.8{\pm}0.9\;g/dL\;vs.\;4.1{\pm}0.3\;g/dL\;P=0.002,\;63.9{\pm}36.4\;mg/dL\;vs.\;100.8{\pm}39.5\;g/dL\;P=0.041$). The mean total protein amount of 24 hour collected urine in the S group were significantly higher than that of the A group($3684.0{\pm}2601.3\;mg/m^2\;vs.\;559.4{\pm}4.6.9\;mg/m^2$, respectively, P=0.001). Hypocomplementemia was observed in 11(61.1%) out of 18 patients at the time of disease onset, 7(87.5%) in the S group and 4(40%) in the A group. However the hypocomplementemia was decreased in 6(33.3%) out of 18 patients at the time of final follow-up, 3(37.5%) in the S group and 3(30%) in the A group. According to the pathologic type, hypocomplementemia was observed 8 patients(61.5%) with type I disease, 1 patients (100%) with type II disease, 2 patients(50%) in type III disease at the disease onset, but 4 patients(30.8%) in type I disease, 1 patient(100%) in type II disease, 1 patient(33.3%) with type III disease at the time of last follow-up. The incidence of cellular crescent formation and tubular atropy. as observed on light microscopy, were higher in the S group compared to the A group. Mean grade of capillary wall thickening and, mesangial proliferation were significantly higher in the S group. Conclusion: MPGN, as diagnosed in patients with only asymptomatic urinary abnormalities, has been increasing, it is more frequent in asymptomatic patients than in patients with presenting symptoms. Our result suggests that MPGN should be considered in the renal biopsy diagnosis regardless of serum $C_3$ level when urinary abnormalities are found by school urinary screening test.