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Benthic marine organisms such as mollusks are often exposed to periodic oxygen deficiency (due to the tidal exposure and/or seasonal expansion of the oxygen-deficient dead zones) and pollution by metals [e.g., cadmium, (Cd)]. These stressors can strongly affect mollusks' survival; however, physiological mechanisms of their combined effects are not fully understood. We studied the effects of Cd exposure on metabolic responses to prolonged anoxia and subsequent recovery in anoxia-tolerant intertidal mollusks Crassostrea virginica (eastern oysters). Anoxia led to an onset of anaerobiosis indicated by accumulation of L-alanine, acetate, and succinate. Prolonged anoxia (for 6 days) caused a decline in the maximum activity of electron transport chain and ADP-stimulated (state 3) oxygen uptake by mitochondria (M[O.sub.2]), but no change in the resting (state 4) M[O.sub.2] of oyster mitochondria, along with a slight but significant reduction of mitochondrial respiratory control ratio. During reoxygenation, there was a significant overshoot of mitochondrial M[O.sub.2] (by up to 70% above the normoxic steady-state values) in control oysters. Mild mitochondrial uncoupling during prolonged shutdown in anoxic tissues and a subsequent strong stimulation of mitochondrial flux during recovery may help to rapidly restore redox status and protect against elevated reactive oxygen species formation in oysters. Exposure to Cd inhibits anaerobic metabolism, abolishes reoxygenation-induced stimulation of mitochondrial M[O.sub.2], and leads to oxidative stress (indicated by accumulation of DNA lesions) and a loss of mitochondrial capacity during postanoxic recovery. This may result in increased sensitivity to intermittent hypoxia and anoxia in Cd-exposed mollusks and will have implications for their survival in polluted estuaries and coastal zones. air exposure; recovery; mitochondrial function; oxidative damage; mollusks doi: 10.1152/ajpregu.00324.2009.

Mapping to chromosome 11 of autosomal dominant nanophthalmos (NNO1 (ital)) with high hyperopia and angle-closure glaucoma is discussed. This developmental ocular disorder, for which ocular examinations of 22 affected members of a large family were done, is uncommon and involves a small eye, in terms of axial length, high hyperopia, high incidence of angle-closure glaucoma and a high lens/eye volume ratio.

We recently showed that the chloroplast small heat-shock protein (chip smHsp) protects photosynthetic electron transport in vitro during heat stress; however, in vivo evidence of the importance of this Hsp to organismal thermotolerance is lacking. Here we report positive relationships between chip smHsp production and organismal thermotolerance among diverse species and ecotypes of Chenopodium album. Positive relationships were also observed between smHsp production and photosynthetic thermotolerance among tomato genotypes differing in heat tolerance and between heat-tolerant wild-type and heat-sensitive mutant genotypes of Agrostis palustris. These results indicate that genetic variation in production of the chip smHsp is an important determinant of whole-plant thermotolerance. We recently showed that the mitochondrial smHsp protects respiratory electron transport in vitro in plants and humans, suggesting that the mitochondrial smHsp is also an important adaptation to stress.

The endogenous production of oxygen-centered free radicals and resulting oxidative damage may occur in tissues exposed to hypoxia, hyperoxia, or hydrogen sulfide. Previous investigations of oxidative damage from these stressors in marine invertebrates have produced conflicting results, perhaps because these studies utilized species that are presumably adapted to these stressors and therefore may not show strong evidence of oxidative damage or antioxidant response. To increase the likelihood of detecting oxidative stress, we examined the effects of these stressors in the surf clam Donax variabilis, which inhabits high-energy sandy beaches and is therefore unlikely to have specific physiological adaptations to these stressors. D. variabilis were exposed to hypoxia (~10 kPa [Po.sub.2]), hyperoxia (~27 kPa [Po.sub.2]), or hydrogen sulfide (~100 [micro]M) for 24-hour experiments in a flow-through system. We used immunochemical analysis and dot blotting to quantify whole-animal expression levels of antioxidant (copper-zinc and manganese superoxide dismutases, glutathione peroxidase), stress (heme oxygenase, ferrochelatase, ubiquitin, glutathione), heat shock (60, 70, GT75, small HSP), and oxidative damage repair proteins (HNE, MutY, and mitochondrial OGG-1). In general, antioxidant proteins and oxidative damage repair proteins increased two- to six-fold (p > 0.01) in all treatment groups in comparison to normoxic controls, with hyperoxic and sulfidic conditions inducing greater responses than hypoxia. Surprisingly, heme oxygenase, ferrochelatase, and sHSP, which have been reported to respond to hypoxia and hyperoxia in mammalian models, did not change significantly. This stress protein response in D. variabilis suggests that these abiotic stressors do induce oxidative damage, particularly in a species not adapted to these conditions.

In the tissues of intertidal invertebrates, endogenous production of oxygen-centered free radicals and resulting oxidative damage may occur during tidal cycles due to hypoxia and subsequent reoxygenation. The cellular response to this oxidative damage is poorly understood. In this study, we evaluated the response of coelomocytes from the intertidal polychaete Glycera dibranchiata to hypoxia/ reoxygenation in vitro. Coelomocytes were collected from 24 worms, resuspended in buffered seawater, and randomly assigned to one of the following treatments (4 worms per treatment): anoxia (6 h), anoxia (6 h) followed by reoxygenation (6 h), anoxia (6 h) followed by reoxygenation (12 h), and normoxia for 6, 12, and 18 h. We used polyacrylamide gel electrophoresis/Western blotting and immunochemical analysis to quantify the levels of the antioxidant enzyme manganese superoxide dismutase (MnSOD), and heat shock protein 70 (Hsp70). Hsp70 was significantly (p < 0.032) decreased in cells treated with anoxia and with anoxia/reoxygenation, in comparison to normoxia-treated cells. This was likely due in large part to an overall decrease in cellular metabolism during anoxia. In contrast, we found that MnSOD levels decreased significantly (p < 0.04) in anoxia-treated cells, but after 12 hours of reoxygenation, MnSOD levels were indistinguishable from normoxia controls. This upregulation of MnSOD during reoxygenation likely is a response to free radical production. The results of this cellular-level short-term, in vitro study complement those reported by Storey and colleagues, who have conducted longer-term whole-animal incubations with hypoxia-tolerant turtles and intertidal marine gastropods.

Coral reefs in the Florida Keys are severely degraded with a reported 38% loss between 1996 and 2000, yet the causes of these devastating declines remain largely unknown. Our long-term studies in the Upper Keys and Biscayne National Park indicate acute stress events affecting physiological condition in species representing different trophic levels in the reef community, one of which was white grunt ( Haemulon plumieri ; Lacépède, 1801). We initiated a preliminary investigation describing cellular physiological stress effects and the possible causes of these stress events using cellular diagnostic profiling coupled with a cursory body-load contaminant chemistry analysis. The cellular biomarker profiles from fish taken from Alina's Reef indicated a toxic response profile that was suggestive of a suicide reaction of the cytochrome P450 2-class as a result of an interaction with a xenobiotic that adversely affects heme metabolism. Elevated levels of damaged porphyrin products were also found in fish from Alina's Reef. Liver loads of anthropogenic contaminants (e.g., pesticides, PCBs) were measured and provided further evidence for possible causative agents. Evaluation and synthesis of each type of data were used to establish a biological effect, develop a mechanism of pathogenicity, and build a profile for possible causative agent(s). [ABSTRACT FROM AUTHOR]