Cytochrome b(561) mediates equilibration of the ascorbate/semidehydroascorbate redox couple across the membranes of secretory vesicles. The cytochrome is reduced by ascorbic acid and oxidized by semidehydroascorbate on either side of the membrane. Treatment with diethyl pyrocarbonate (DEPC) inhibits reduction of the cytochrome by ascorbate, but this activity can be restored by subsequent treatment with hydroxylamine, suggesting the involvement of an essential histidine residue. Moreover, DEPC inactivates cytochrome b(561) more rapidly at alkaline pH, consistent with modification of a histidine residue. DEPC does not affect the absorption spectrum of cytochrome b(561) nor does it change the midpoint reduction potential, confirming that histidine modification does not affect the heme. Ascorbate protects the cytochrome from inactivation by DEPC, indicating that the essential histidine is in the ascorbate-binding site. Further evidence for this is that DEPC treatment inhibits oxidation of the cytochrome by semidehydroascorbate but not by ferricyanide. This supports a reaction mechanism in which ascorbate loses a hydrogen atom by donating a proton to histidine and transferring an electron to the heme.
The purpose of this study was to evaluate the responses of coronary and pulmonary arteries to the generation of superoxide (O2.) via organic redox complex formation between ascorbic acid and imidazole. Imidazole facilitates the transfer of electrons from ascorbic acid to O2 resulting in the generation of O2. Using a Clark style electrode, oxygen levels were monitored in solutions of ascorbic acid and imidazole and decreasing oxygen levels were used as an indication of O2. generation. In another series of experiments, small rings of porcine coronary and pulmonary arteries were dissected, mounted in isolated organ baths, and administered increasing concentrations (10−8–10−3 M) of ascorbic acid, glycine, imidazole, or ascorbic acid and imidazole. Vascular responses were recorded as changes in tension. The combination of ascorbic acid and imidazole, but not ascorbic acid or glycine, caused a significant vasoconstriction in both coronary and pulmonary arteries. Imidazole induced vasoconstriction in coronary arteries. Taken together, these results suggest that ascorbic acid in the presence of imidazole may increase O2. production resulting in an increase in tension in coronary and pulmonary arteries. This research was supported by a Grand Valley State University Research Grant‐in‐Aid.
The objective of this study was to evaluate the role of superoxide (O2•−) resulting from the reaction between imidazole and vitamin C in altering the vascular reactivity of coronary arteries. It was hypothesized that a potential non‐enzymatic redox reaction between vitamin C and imidazole results in the production of O2•− and alters vascular reactivity. Left anterior descending coronary arteries (LAD) from porcine hearts were dissected, mounted in organ baths and passively loaded with 1.5 g of tension. Following a 5‐hour equilibration with control (Krebs‐Henseleit solution), vitamin C (2mM), imidazole (200mM), or combination of vitamin C and imidazole, LADs were treated with increasing concentrations of potassium chloride (KCl) and sodium nitroprusside (SNP) to assess changes in vascular reactivity. Incubation with the combination of vitamin C and imidazole as well as imidazole alone attenuated vascular responses to KCl and SNP. To detect the presence of O2•− in coronary arteries, a fluorescent dye‐based dihydorethidine (DHE) assay was utilized. An increase in the O2•− levels was observed in the arteries incubated with vitamin C and imidazole. The results from these studies may provide basic information on non‐enzymatic sources of superoxide in the vasculature and their effect on coronary artery function. This research was supported by a Grand Valley State University Presidential Grant.
This workshop focuses on the benefits and challenges of incorporating digital education technology into 21st century undergraduate science education. Students and faculty alike are adapting to a new, more technologically driven paradigm of pedagogy in the ‘classroom.’ In The College of 2020: Students (2009), Van Der Werf and Sabatier predict this shift will continue in a variety of manners: greater student access of online courses, improved access via portable computing devices, greater connectivity and creativity from colleges, personalization of education, exploring concepts through games and simulations, among other pedagogical changes. Scientific organizations, publishing companies, and technology companies are driving many of these technological innovations. Research is starting to emerge on the pedagogical effectiveness of digital education resources, although no clear, definitive relationship has been identified. The goals of this workshop are to discuss: 1) how digital education resources can be leveraged to complement and enhance traditional science education pedagogical approaches, and 2) preliminary results of studies identifying the resources anatomy and physiology students find most effective for studying and learning. Digital content from McGraw‐Hill Higher Education as utilized by two faculty members in their A&P courses will be discussed as part of the preliminary research.
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