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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Boink A B, Wemer J, Meulenbelt J, Vaessen H A, de Wildt D J

Laboratory of Toxicology, National Institute of Public Health and Environmental Protection, Bilthoven, The Netherlands.

Hum Exp Toxicol. 1994 Mar;13(3):149-55. doi: 10.1177/096032719401300302.

Fluoride intoxication leads to sudden cardiac death which has been assumed to result from the accompanying severe hypocalcaemia. The aim of this study has been to investigate the suggestion that fluorapatite formation rather than CaF2 precipitation is responsible for this low calcium. 2. Measurements of free Ca2+ and F- ion concentrations in HEPES buffered solutions containing F-, Ca2+, and phosphate ions at different concentrations in the absence and presence of hydroxyapatite showed that the presence of hydroxyapatite enhanced the decrease of Ca2+ and F- concentration. 3. The ratio of Ca2+:F- clearance was 5:1 which is consistent with formation of fluorapatite. These results support the hypothesis that hydroxyapatite acts as a nucleation catalyst for fluorapatite formation and this process is responsible for the hypocalcaemia induced by fluoride intoxication. 4. The proposed mechanism explains also the metabolic acidosis which is frequently seen in cases of fluoride intoxication.

氟中毒会导致心源性猝死，一般认为这是由伴随的严重低钙血症所致。本研究的目的是调查以下观点：造成这种低钙情况的原因是氟磷灰石的形成，而非氟化钙沉淀。2. 在有无羟基磷灰石的情况下，对含有不同浓度氟离子、钙离子和磷酸根离子的HEPES缓冲溶液中的游离钙离子和氟离子浓度进行测量，结果表明，羟基磷灰石的存在加剧了钙离子和氟离子浓度的降低。3. 钙离子与氟离子清除率之比为5:1，这与氟磷灰石的形成相符。这些结果支持了以下假设：羟基磷灰石作为氟磷灰石形成的成核催化剂，这一过程导致了氟中毒引起的低钙血症。4. 所提出的机制也解释了氟中毒病例中常见的代谢性酸中毒。

Boink A B, Wemer J, Meulenbelt J, Vaessen H A, de Wildt D J

Laboratory of Toxicology, National Institute of Public Health and Environmental Protection, Bilthoven, The Netherlands.

Hum Exp Toxicol. 1994 Mar;13(3):149-55. doi: 10.1177/096032719401300302.

Fluoride intoxication leads to sudden cardiac death which has been assumed to result from the accompanying severe hypocalcaemia. The aim of this study has been to investigate the suggestion that fluorapatite formation rather than CaF2 precipitation is responsible for this low calcium. 2. Measurements of free Ca2+ and F- ion concentrations in HEPES buffered solutions containing F-, Ca2+, and phosphate ions at different concentrations in the absence and presence of hydroxyapatite showed that the presence of hydroxyapatite enhanced the decrease of Ca2+ and F- concentration. 3. The ratio of Ca2+:F- clearance was 5:1 which is consistent with formation of fluorapatite. These results support the hypothesis that hydroxyapatite acts as a nucleation catalyst for fluorapatite formation and this process is responsible for the hypocalcaemia induced by fluoride intoxication. 4. The proposed mechanism explains also the metabolic acidosis which is frequently seen in cases of fluoride intoxication.

氟中毒会导致心源性猝死，一般认为这是由伴随的严重低钙血症所致。本研究的目的是调查以下观点：造成这种低钙情况的原因是氟磷灰石的形成，而非氟化钙沉淀。2. 在有无羟基磷灰石的情况下，对含有不同浓度氟离子、钙离子和磷酸根离子的HEPES缓冲溶液中的游离钙离子和氟离子浓度进行测量，结果表明，羟基磷灰石的存在加剧了钙离子和氟离子浓度的降低。3. 钙离子与氟离子清除率之比为5:1，这与氟磷灰石的形成相符。这些结果支持了以下假设：羟基磷灰石作为氟磷灰石形成的成核催化剂，这一过程导致了氟中毒引起的低钙血症。4. 所提出的机制也解释了氟中毒病例中常见的代谢性酸中毒。