Search

© 2015 John Wiley & Sons Ltd. Despite the abundance of literature on organismal responses to multiple environmental stressors, most studies have not matched the timing of experimental manipulations with the temporal pattern of stressors in nature. We test the interactive effects of diel-cycling hypoxia with both warming and decreased salinities using ecologically realistic exposures. Surprisingly, we found no evidence of negative synergistic effects on Olympia oyster growth; rather, we found only additive and opposing effects of hypoxia (detrimental) and warming (beneficial). We suspect that diel-cycling provided a temporal refuge that allowed physiological compensation. We also tested for latent effects of warming and hypoxia to low-salinity tolerance using a seasonal delay between stressor events. However, we did not find a latent effect, rather a threshold survival response to low salinity that was independent of early life-history exposure to warming or hypoxia. The absence of synergism is likely the result of stressor treatments that mirror the natural timing of environmental stressors. We provide environmental context for laboratory experimental data by examining field time series environmental data from four North American west coast estuaries and find heterogeneous environmental signals that characterize each estuary, suggesting that the potential stressor exposure to oysters will drastically differ over moderate spatial scales. This heterogeneity implies that efforts to conserve and restore oysters will require an adaptive approach that incorporates knowledge of local conditions. We conclude that studies of multiple environmental stressors can be greatly improved by integrating ecologically realistic exposure and timing of stressors found in nature with organismal life-history traits.

The effect of a high vitamin E diet on the early stages of colon carcinogenesis and on the proliferative indexes in the colon and in the prostate glands was investigated in rats. F344 male rats were injected with azoxymethane (AOM, 15 mg/kg sc). One week later, animals were randomly allocated into two dietary groups (n = 8 rats/group): normal vitamin E (50 IU/kg diet) and high vitamin E (200 IU/kg diet). The basal diet was the AIN-76 diet modified to contain high corn oil (23% wt/wt). After eight weeks of feeding, concentrations of vitamin E in plasma, liver, and prostate were analyzed. Enumeration of aberrant crypt foci (ACF) in colons and proliferative indexes of colons and prostate glands were determined. The total number of ACF and the average number of aberrant crypts (AC) per focus were similar in both dietary groups. ACF were classified as small (1-3 crypts/focus), medium (4-6 crypts/focus), or large (or = 7 crypts/focus). Only the ACF in the small category showed a significant treatment effect, with values being lower in the high vitamin E group than in the control group (por = 0.05). No significant difference was observed in colonic proliferative indexes assessed by enumeration of metaphase cells, S phase cells, or cells exhibiting proliferative cell nuclear antigen (PCNA). The PCNA labeling index in the prostate glands and the activity of prostatic acid phosphatase in plasma were higher in high vitamin E-fed rats (por = 0.05) than in control animals. The present study demonstrates that additional vitamin E does not inhibit the induction and growth of ACF; also it enhances the proliferative status of the prostate glands.