On the Nature of Some Selenium Losses from Soils and Waters

Selenium is of interest to the animal nutritionists and to the biochemist from two standpoints. In some areas of the world it occurs in soils in excesses, and the plants growing in these soils contain levels of the element that are toxic to livestock that consume the plants. On the other hand, selenium appears to be essential to the well-being of certain animals, at least under some feeding regimens, and in a number of areas the soils produce feeds that are deficient in the element (48). In either case, an understanding of the cycling of selenium in nature is essential to the explanation of why certain soils produce plants deficient in the element while others produce plants which contain an excess. Such an explanation should be helpful, not only in the matter of mapping these areas, but also in terms of managing the lands for optimum production. Reviews by Allaway et al. (2) and by Olson (41) have dealt with the cycling of selenium in nature and have pointed to the need for further investigation of certain phases of it. The possible role of micro-organisms, for instance, has not been given adequate consideration. In part, having no adequate analytical method has contributed to the deficiency of information on this matter, the methods used until recently lacking the sensitivity and perhaps the accuracy required for this type of work. Recent advances in methods for the analysis of biological materials for selenium have opened the possibilities for further work, and it was the purpose of the investigations discussed here to study and adapt the newer methods of use in preliminary studies to evaluate the possible role of microorganisms in cycling selenium in soils and waters. The radioisotope, Se75, while extremely helpful in certain types of studies, cannot be substituted for the many forms of selenium that occur naturally in soils

Aging impairs myocardial fatty acid and ketone oxidation and modifies cardiac functional and metabolic responses to insulin in mice

Aging presumably initiates shifts in substrate oxidation mediated in part by changes in insulin sensitivity. Similar shifts occur with cardiac hypertrophy and may contribute to contractile dysfunction. We tested the hypothesis that aging modifies substrate utilization and alters insulin sensitivity in mouse heart when provided multiple substrates. In vivo cardiac function was measured with microtipped pressure transducers in the left ventricle from control (4–6 mo) and aged (22–24 mo) mice. Cardiac function was also measured in isolated working hearts along with substrate and anaplerotic fractional contributions to the citric acid cycle (CAC) by using perfusate containing 13C-labeled free fatty acids (FFA), acetoacetate, lactate, and unlabeled glucose. Stroke volume and cardiac output were diminished in aged mice in vivo, but pressure development was preserved. Systolic and diastolic functions were maintained in aged isolated hearts. Insulin prompted an increase in systolic function in aged hearts, resulting in an increase in cardiac efficiency. FFA and ketone flux were present but were markedly impaired in aged hearts. These changes in myocardial substrate utilization corresponded to alterations in circulating lipids, thyroid hormone, and reductions in protein expression for peroxisome proliferator-activated receptor (PPAR)α and pyruvate dehydrogenase kinase (PDK)4. Insulin further suppressed FFA oxidation in the aged. Insulin stimulation of anaplerosis in control hearts was absent in the aged. The aged heart shows metabolic plasticity by accessing multiple substrates to maintain function. However, fatty acid oxidation capacity is limited. Impaired insulin-stimulated anaplerosis may contribute to elevated cardiac efficiency, but may also limit response to acute stress through depletion of CAC intermediates