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Roots as a site of hydrogen sulfide uptake in the hydrocarbon seep vestimentiferan Lamellibrachia sp.
The characteristics of the root suggest that it reaches down to the higher sulfide levels present in the deeper sediment and that it functions to increase the surface area available for sulfide uptake in a manner analogous to a respiratory organ.
Multiple Mechanisms Provide Tolerance to Environmental Sulfide in Urechis caupo
It is concluded that sulfide tolerance in U. caupo is due primarily to the sulfide oxidation activity of the coelomic fluid and that the specialized integument and hindgut protect the metabolically active, sulfide-exposed epithelial cells.
Oxygen consumption in weakly electric Neotropical fishes
O2 consumption rate was not dependent on EOD type, but maintenance of “scan swimming” (continuous forwards and backwards swimming) increased O2 consumption 2.83±0.49-fold, suggesting that the increased metabolic cost of scan swimming could restrict gymnotiforms with wave-type EODs from hypoxic habitats.
Autophagy in the heart and liver during normal aging and calorie restriction.
Calorie restriction may mediate some of its beneficial effects by stimulating autophagy in the heart, indicating the potential for cardioprotective therapies.
Hydrogen Sulfide Induces Oxidative Damage to RNA and DNA in a Sulfide‐Tolerant Marine Invertebrate
Worms exposed in vivo to sulfide acquired elevated oxidative damage to RNA and DNA in both coelomocytes and body wall tissue, suggesting that sulfide can be an environmental mutagen in sulfide‐tolerant invertebrates.
Enzymatic hydrogen sulfide production in marine invertebrate tissues.
New Mediterranean Biodiversity Records (July 2016)
This contribution forms part of a series of collective articles published regularly in Mediterranean Marine Science that report on new biodiversity records from the Mediterranean basin. The current
Mitochondrial depolarization following hydrogen sulfide exposure in erythrocytes from a sulfide-tolerant marine invertebrate
It is indicated that sulfide exposure causes mitochondrial depolarization in cells of a sulfide-tolerant annelid, and that this effect, which differs from the actions of other COX inhibitors, may be via increased free radical damage.