ABSTRACT, we measured the sensitivity of muscles and neurons to ROS attack. Neural outputs from flight motor neurons and sensory neurons were unchanged in Sod2 n283 and the entire neural circuitry between the giant fiber (GF) and the dorsal longitudinal muscles (DLM) showed no overt defect due to elevated ROS. Such insensitivity of neurons to mitochondrial superoxides was further established through neuronal expression of SOD2, which failed to improve survival or locomotive ability of Sod2 n283 . On the other hand, ultrastructural analysis of Sod2 n283 muscles revealed fewer mitochondria and reduced muscle ATP production. By targeting the SOD2 expression to the muscle we demonstrate that the early mortality phenotype of Sod2 n283 can be ameliorated along with signs of improved mobility. In summary, muscles appear to be more sensitive to superoxide attack relative to the neurons and such overt phenotypes observed in SOD2-deficient animals can be directly attributed to the muscle.
A 17-year-old girl swallowed at least 50 Duroferon durettep. Each tablet contains ferrous sulphate equivalent to 0.1 g Fe2+. Thus, a total of 5 g Fez+ was ingested. Vitamin K-dependent coagulation factors dropped within the next hours to very low levels. Thrombotest showed less than 3% of normal coagulation activity 8 h after oral intake. Recovery was uneventful except for laboratory evidence of transient liver damage. The rapidity by which the early coagulation deficiencies developed and the lack of evidence of disseminated intravascular coagulation suggested a direct effect of iron on coagulation factors. In vitro studies confirmed that iron in concentrations that may have been attained in vivo, altered the functional activity of several coagulation factors. Monitoring the vitamin K-dependent coagulation factors may be a simple and useful parameter in acute iron intoxication.
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