Exposure to crude oil micro-droplets causes reduced food uptake in copepods associated with alteration in their metabolic profiles.

Acute oil spills and produced water discharges may cause exposure of filter-feeding pelagic organisms to micron-sized dispersed oil droplets. The dissolved oil components are expected to be the main driver for oil dispersion toxicity; however, very few studies have investigated the specific contribution of oil droplets to toxicity. In the present work, the contribution of oil micro-droplet toxicity in dispersions was isolated by comparing exposures to oil dispersions (water soluble fraction with droplets) to concurrent exposure to filtered dispersions (water-soluble fractions without droplets). Physical (coloration) and behavioral (feeding activity) as well as molecular (metabolite profiling) responses to oil exposures in the copepod Calanus finmarchicus were studied. At high dispersion concentrations (4.1-5.6mg oil/L), copepods displayed carapace discoloration and reduced swimming activity. Reduced feeding activity, measured as algae uptake, gut filling and fecal pellet production, was evident also for lower concentrations (0.08mg oil/L). Alterations in metabolic profiles were also observed following exposure to oil dispersions. The pattern of responses were similar between two comparable experiments with different oil types, suggesting responses to be non-oil type specific. Furthermore, oil micro-droplets appear to contribute to some of the observed effects triggering a starvation-type response, manifested as a reduction in metabolite (homarine, acetylcholine, creatine and lactate) concentrations in copepods. Our work clearly displays a relationship between crude oil micro-droplet exposure and reduced uptake of algae in copepods.

Oxidative capacity interacts with oxygen delivery to determine maximal O(2) uptake in rat skeletal muscles in situ.

Based on proportional changes in V(O(2))(,max) with alterations in O(2) delivery, it is widely held that O(2) availability limits V(O(2))(,max). In contrast, reductions in V(O(2))(,max) are also seen when mitochondrial oxidative capacity is reduced. Taken collectively, these prior results are consistent with the notion that there is not a single-step limitation to V(O(2))(,max). We used a pump-perfused rat hindlimb model to test the hypothesis that combining moderate reductions in O(2) delivery and mitochondrial oxidative capacity would yield a greater reduction in V(O(2))(,max) than seen when performing each intervention independently, demonstrating an interaction between O(2) supply and mitochondrial oxidative capacity in determining V(O(2))(,max). Four groups of animals were studied: two in high O(2) delivery conditions (hindlimb O(2) delivery: 88 +/- 1 micromol O(2) min(-1); mean +/- S.E.M.) and two in moderately reduced O(2) delivery conditions (66 +/- 2 micromol O(2) min(-1)). One group at each level of O(2) delivery was treated with 0.1 microM myxothiazol to reduce mitochondrial oxidative capacity via competitive inhibition of NADH cytochrome c reductase. V(O(2))(,max) in control animals (no myxothiazol) was 29 % lower in the moderately reduced O(2) delivery group (592 +/- 24 mmol O(2) min(-1) (100 g)(-1)); P < 0.05) than in the high O(2) delivery group (833 +/- 63 micromol O(2) min(-1) (100 g)(-1)). Similarly, V(O(2))(,max) was reduced by 29 % (594 +/- 22 micromol O(2) min(-1) (100 g)(-1)); P < 0.05) in myxothiazol-treated animals in high O(2) delivery conditions compared to control animals in high O(2) delivery conditions. When myxothiazol treatment was combined with moderately reduced O(2) delivery, V(O(2))(,max) was reduced by an additional 18 % (484 +/- 21 micromol O(2) min(-1) (100 g)(-1)); P < 0.05) compared to either intervention performed independently. These results show that O(2) supply and mitochondrial oxidative capacity interact to determine V(O(2))(,max).