Markovac J, Goldstein G W
Department of Pediatrics, University of Michigan Medical School, Ann Arbor 48109-0570.
Nature. 1988 Jul 7;334(6177):71-3. doi: 10.1038/334071a0.
Recent growth studies in children suggest that there is no threshold for adverse effects from the universal exposure to inorganic lead. The biochemical mechanisms mediating low-level toxicity are unclear, but in several biological systems, lead alters calcium-mediated cellular processes and may mimic calcium in binding to regulatory proteins. Here we present evidence that lead stimulates diacylglycerol-activated calcium and phospholipid-dependent protein kinase, protein kinase C, partially purified from rat brain. Picomolar concentrations of lead are equivalent to micromolar calcium in kinase activation, so this regulatory enzyme is sensitive to the lead levels expected from current environmental exposure.
近期针对儿童的生长研究表明，普遍接触无机铅不存在不良反应阈值。介导低水平毒性的生化机制尚不清楚，但在多个生物系统中，铅会改变钙介导的细胞过程，并且可能在与调节蛋白结合时模拟钙的作用。在此，我们提供证据表明，铅可刺激从大鼠脑中部分纯化得到的二酰基甘油激活的钙和磷脂依赖性蛋白激酶，即蛋白激酶C。皮摩尔浓度的铅在激酶激活方面等同于微摩尔浓度的钙，因此这种调节酶对当前环境暴露预期的铅水平敏感。
