• KOREAN JOURNAL OF PACKAGING SCIENCE & TECHNOLOGY
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• v.28 no.3
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• pp.175-182
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• 2022

Heavy metals can be intentionally or unintentionally introduced into plastic food utensils, containers, and packaging (PFUCP) as additives or contaminants, which can be ingested with food by humans. Here, seven-heavy metals (lead, cadmium, nickel, chromium, antimony, copper, and manganese) with toxicity concerns were selected, and risk assessment was done by establishing their migration from 137 PFUCP products made of 16 materials distributed in Korea. Migration of heavy metals was examined by applying 4% acetic acid as a food simulant (70℃, 30 minutes) to the PFUCP products. Inductively coupled plasma mass spectrometry (ICP-MS) was employed for the analysis of migrated heavy metals, and the reliability of quantitative results was confirmed by checking linearity, LOD, LOQ, recovery, precision, and expanded uncertainty. As a result of monitoring, heavy metals were detected at a level of non-detection to 8.76 ± 11.87 ㎍/L and most of the heavy metals investigated were only detected at trace amounts of less than 1 ㎍/L on average. However, antimony migrated from PET products was significantly higher than other groups. Risk assessment revealed that all the heavy metals investigated were safe with a margin of exposure above 311. Collectively, we demonstrated that heavy metals migrated from PFUCP products distributed in Korea appear to be within the safe range.

• Journal of the Korean Society of Food Science and Nutrition
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• v.35 no.4
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• pp.464-469
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• 2006

This study was conducted to evaluate a knowledge on food components of muscle and adductor muscle of pearl oyster (Pinctada fucata martensii) as pearl processing byproducts. The concentrations of mercury and chromium as heavy metal were not detected in both pearl oyster muscle and adductor muscle, and those of cadmium and lead were 0.06 ppm and 0.11 ppm in only pearl oyster muscle, respectively. Thus, the heavy metal levels of pearl processing byproducts were below the reported safety limits. The volatile basic nitrogen (VBN) content and pH of pearl oyster muscle were 11.6 mg/100g and 6.31 and those of abductor muscle were 8.6 mg/100 g and 6.33, respectively. It was concluded that pearl oyster muscle and adductor muscle might not invoke health risk in using food resource. The contents of crude protein (16.5%) and total amino acid (15,691 mg/100 g) of adductor muscle were higher than those of muscle (11.2% and 10,131 mg/100 g) and oyster (12.1% and 11,213 mg/100 g) as a control. The contents of calcium and phosphorus were 95.4 mg/100 g and 116.0 mg/100 g in muscle, 75.2 mg/100g and 148.1 mg/100 g in adductor muscle, respectively. The calcium level based on phosphorus was a good ratio for absorbing calcium. The free amino acid contents and taste values were 635.5 mg/100 g and 40.2 in muscle, and 734.9 mg/100 g and 24.1 in adductor muscle, respectively, but that (882.8 mg/100 g and 40.2) of oyster was higher than those of pearl processing byproducts. Based on the results of physicochemical and nutritional properties, pearl oyster muscle and adductor muscle can be utilized as a food resource.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1265-1276
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• 1998

Background : Nitric oxide(NO) is an endogenously produced free radical that plays an important role in regulating vascular tone, inhibition of platelet aggregation and white blood cell adhesion to endothelial cells, and host defense against infection. The highly reactive nature of NO with oxygen radicals suggests that it may either promote or reduce oxidant-induced cell injury in several biological pathways. Oxidant injury and interactions between pulmonary vascular endothelium and leukocytes are important in the pathogenesis of acute lung injury, including acute respiratory distress syndrome(ARDS). In ARDS, therapeutic administration of NO is a clinical condition providing exogenous NO in oxidant-induced endothelial injury. The role of exogenous NO from NO donor or the suppression of endogenous NO production was evaluated in oxidant-induced endothelial injury. Method : The oxidant injury in cultured rat lung microvascular endothelial cells(RLMVC) was induced by hydrogen peroxide generated from glucose oxidase(GO). Cell injury was evaluated by $^{51}$chromium($^{51}Cr$) release technique. NO donor, such as S-nitroso-N-acetylpenicillamine(SNAP) or sodium nitroprusside(SNP), was added to the endothelial cells as a source of exogenous NO. Endogenous production of NO was suppressed with N-monomethyl-L-arginine(L-NMMA) which is an NO synthase inhibitor. L-NMMA was also used in increased endogenous NO production induced by combined stimulation with interferon-$\gamma$(INF-$\gamma$), tumor necrosis factor-$\alpha$(TNF-$\alpha$), and lipopolysaccharide(LPS). NO generation from NO donor or from the endothelial cells was evaluated by measuring nitrite concentration. Result : $^{51}Cr$ release was $8.7{\pm}0.5%$ in GO 5 mU/ml, $14.4{\pm}2.9%$ in GO 10 mU/ml, $32.3{\pm}2.9%$ in GO 15 mU/ml, $55.5{\pm}0.3%$ in GO 20 mU/ml and $67.8{\pm}0.9%$ in GO 30 mU/ml ; it was significantly increased in GO 15 mU/ml or higher concentrations when compared with $9.6{\pm}0.7%$ in control(p < 0.05; n=6). L-NMMA(0.5 mM) did not affect the $^{51}Cr$ release by GO. Nitrite concentration was increased to $3.9{\pm}0.3\;{\mu}M$ in culture media of RLMVC treated with INF-$\gamma$ (500 U/ml), TNF-$\alpha$(150 U/ml) and LPS($1\;{\mu}g/ml$) for 24 hours ; it was significantly suppressed by the addition of L-NMMA. The presence of L-NMMA did not affect $^{51}Cr$ release induced by GO in RLMVC pretreated with INF-$\gamma$, TNF-$\alpha$ and LPS. The increase of $^{51}Cr$ release with GO(20 mU/ml) was prevented completely by adding 100 ${\mu}M$ SNAP. But the add of SNP, potassium ferrocyanate or potassium ferricyanate did not protect the oxidant injury. Nitrite accumulation was $23{\pm}1.0\;{\mu}M$ from 100 ${\mu}M$ SNAP at 4 hours in phenol red free Hanks' balanced salt solution. But nitrite was not detectable from SNP upto 1 mM The presence of SNAP did not affect the time dependent generation of hydrogen peroxide by GO in phenol red free Hanks' balanced salt solution. Conclusion : Hydrogen peroxide generated by GO causes oxidant injury in RLMVC. Exogenous NO from NO donor prevents oxidant injury, and the protective effect may be related to the ability to release NO. These results suggest that the exogenous NO may be protective on oxidant injury to the endothelium.

• The Korean Journal of Nuclear Medicine
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• v.4 no.1
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• pp.19-26
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• 1970

1. Sixteen normal healthy subjects free from occult blood in the stool were selected and administered with their $^{51}Cr$ labeled own blood via duodenal tube and the recovery rate of radioactivity in feces and urine was measured. The average fecal recovery rate was 90.7 per cent ($85.7{\sim}97.7%$) of the administered radioactivity, and the average urinary excretion rate was 0.8 per cent ($0.5{\sim}1.5%$) 2. There was a close correlation between the amount of blood administered and the recovery rate from the feces; the more the blood administered, the higher the recovery rate was. It was also found that the administration of the tagged blood in the amount exceeding 15ml was suitable for measuring the radioactivity in the stools. 3. In five normal healthy subjects whose circulating erythrocytes had been tagged with $^{51}Cr$, there was little fecal excretion of radioactivity (average 0.9 ml of blood per day). This excretion is not related to hemorrhage and the main route of excretion of such an negligible radioactivity was postulated as gastric juice and bile. 4. A comparison of the radioactivity in the blood and feces of the patients with $^{51}Cr$ labeled erythrocytes seems to be a valid way of estimating intestinal blood loss.