Are vitamins A and E associated with persistent organic pollutants and fatty acids in the blubber of highly contaminated killer whales (Orcinus orca) from Greenland?

We quantified blubber concentrations of vitamins A (retinol) and E (α-tocopherol) and evaluated associations with persistent organic pollutants (ΣPOPs) in 14 highly-contaminated killer whales (Orcinus orca) sampled in Greenland from 2012 to 2014. We considered the influence of blubber depth, sex/age class and diet (based on biomass % of major fatty acids) in these relationships. Blubber concentrations of vitamin A averaged 34.1 ±â€¯4.7 µg g-1 wet weight (ww) and vitamin E averaged 35.6 ±â€¯4.4 µg g-1 ww. Although overall vitamin A concentrations did not vary between inner (closer to the muscle) and outer (closer to the skin) blubber layer or between sub-adults and adult females, concentrations in the outer layer of sub-adults were lower compared to the outer layer of adult females (p = 0.03). Outer layer may therefore reflect age accumulation of vitamin A, while in the more active inner layer, age effects might be masked by metabolic needs such as lactation. Neither diet nor ΣPOPs affected vitamin A variation, suggesting this vitamin is highly regulated in the body. Given the high exposures in these killer whales, vitamin A might not be a sensitive biomarker for POPs adverse effects. Vitamin E concentrations were significantly higher in inner compared to outer layer (p < 0.001), likely associated with blubber composition, suggesting that biopsies may not fully represent vitamin E concentrations in blubber. Age-accumulation of vitamin E also occurred with higher concentrations in adult females compared to sub-adults, independent of blubber depth (p < 0.01). Diet, ΣPOPs, and an interaction between these two variables significantly affected vitamin E variation in inner blubber, explaining 91% of this variation. The negative relationship between ΣPOPs (especially Σdichlorodiphenyltrichloroethane (DDT) and Σchlordanes in outer layers) and vitamin E was observed only in killer whales with a diet poorer in polyunsaturated fatty acids, suggested that killer whales feeding more consistently on marine mammals in Arctic environments over a fish-based diet, may be at higher risk of POP-induced disruption in vitamin E homeostasis. Considering diet is therefore important to understand the potential effects of elevated contaminant exposures on levels of certain essential nutrients, i.e., vitamin E, in killer whales.

Fracture toughness and load relaxation of dentin bonding resin systems.

OBJECTIVES: The fracture toughness (KIC) and load relaxation of four dentin bonding resins were determined to characterize some of the mechanical properties of these materials after polymerization. METHODS: A total of 40 single-edge notch bar specimens were fabricated, 10 each of four commercially available brands, and subjected to three-point bending until fracture, as described in ASTM Standard E399-83 (1991a). The critical stress intensification factor, KIC, was derived for each specimen and compared by analysis of variance and Scheffé's multiple comparisons test (p < 0.01). To study the load relaxation characteristics, five rectangular specimens (without notches) of each brand were subjected to three-point loading until a predetermined limiting load value was reached. The test load was allowed to relax for 4 min, after which the specimen was unloaded to the zero load condition, and the load was allowed to build up on its own accord for 3 min. Load relaxation values were measured from the chart, and the mean percent load drop was calculated. The load relaxation data were compared using analysis of variance and Scheffé's multiple comparisons test (p < 0.05). RESULTS: The fracture toughness (KIC) values of the four adhesive resins studied in this investigation ranged from 0.37-0.94 MPa.m0.5 and were statistically different from each other (p < 0.001). The load relaxation values were found to be greatest within the first 0.5 min, with the total load relaxation of the four bonding agents ranging from 16%-30%. Two of the materials studied showed significantly different short-term load relaxation behavior than the other two resins (p < 0.05). SIGNIFICANCE: Bonding agents can be implicated as one of the factors that weaken the interface between the dentin and the composite restorative material. These materials are capable of a rapid short-term response, demonstrating significant load relaxation in the first 0.5 min after loading.

The isolation and characterization of glutamine-requiring strains of Escherichia coli K12.

Mutants of Escherichia coli K12 requiring glutamine as a nitrogen source were isolated, and characterized as lacking glutamine synthetase activity. Temperature sensitive revertants of one of the mutants had a heat labile glutamine synthetase, while temperature insensitive revertants had a glutamine synthetase which was thermostable in vitro, indicating that the mutation was in the structural gene for the enzyme. All of the mutations mapped in the same region of the chromosome suggesting that they might all be in the same gene. The glutamine synthetase gene (gln) was located on the E. coli chromosome by conjugation and P1-mediated transduction at minute 77. The gln gene cotransduced with the genes for oleate degradation (old), and the genes for L-rhamnose utilization (rha). The most probable gene order is old-gln-rha.

Enhanced pulmonary toxicity in copper-deficient rats exposed to hyperoxia.

The antioxidant enzyme superoxide dismutase (SOD) found in the cytosol of eucaryotic cells and the plasma protein ceruloplasmin are copper containing proteins though to be important in providing protection from oxygen toxicity. To investigate the hypothesis that copper deficiency in the rat could result in decreased lung SOD activity and plasma ceruloplasmin concentration resulting in increased susceptibility to O2 lung damage, we performed a series of experiments exposing copper-deficient and control rats to normobaric and hyperbaric hyperoxia. Lung SOD activity in the copper-deficient rats was found to be 56% of control and ceruloplasmin content was 6% of control. The copper-deficient rats exhibited increased mortality and enhanced pulmonary toxicity as evidenced by increased pathologic damage and lung edema during the normobaric exposure to 85% O2. Copper-deficient animals also showed increased susceptibility to a hyperbaric exposure of 4 ata of 100% O2 with a decreased time of survival. The copper-deficient rat represents a new model for the study of oxidant injury.