Surface ultrastructural changes in the gills of sockeye salmon (teleostei: Oncorhynchus nerka) during seawater transfer: Comparison of successful and unsuccessful seawater adaptation

Sockeye salmon were transferred rapidly from freshwater to seawater and the changes in gill morphology, in particular the distribution and sizes of chloride and mucous cells on the afferent filamental surface examined. Salmon that successfully adapted to seawater were compared with salmon that did not adapt to seawater and died as a consequence of osmoregulatory failure. The number of mucus cells (density), determined from scanning electron microscopy, increased significantly after seawater challenge. A greater increase in mucus cell density occurred in the salmon that failed to adapt to seawater. Light microscopy of transverse sections of gills detected no difference in mucus cell numbers after seawater challenge. It is proposed that mucus cells that lie just beneath the gill epithelium are activated in response to the seawater challenge, and migrate and open onto the epithelium. Freshwater-adapted salmon that had low densities of chloride cells prior to the seawater challenge failed to adapt, whereas salmon that had high densities of chloride cells adapted successfully to seawater. In the latter, the density of chloride cells on the afferent surface decreased after 30 days in seawater. The apical surface of the chloride cells of freshwater-adapted sockeye were either smooth or covered with microvilli. A greater proportion of microvilli-covered chloride cells occurred in the freshwater-adapted salmon that subsequently adapted to seawater.     

Mechanism of the persistent sodium current activator veratridine-evoked Ca2+ elevation: implication for epilepsy

Although the role of Na⁺ in several aspects of Ca²⁺ regulation has already been shown, the exact mechanism of intracellular Ca²⁺ concentration ([Ca²⁺]_i) increase resulting from an enhancement in the persistent, non‐inactivating Na⁺ current (I_Na,P), a decisive factor in certain forms of epilepsy, has yet to be resolved. Persistent Na⁺ current, evoked by veratridine, induced bursts of action potentials and sustained membrane depolarization with monophasic intracellular Na⁺ concentration ([Na⁺]_i) and biphasic [Ca²⁺]_i increase in CA1 pyramidal cells in acute hippocampal slices. The Ca²⁺ response was tetrodotoxin‐ and extracellular Ca²⁺‐dependent and ionotropic glutamate receptor‐independent. The first phase of [Ca²⁺]_i rise was the net result of Ca²⁺ influx through voltage‐gated Ca²⁺ channels and mitochondrial Ca²⁺ sequestration. The robust second phase in addition involved reverse operation of the Na⁺–Ca²⁺ exchanger and mitochondrial Ca²⁺ release. We excluded contribution of the endoplasmic reticulum. These results demonstrate a complex interaction between persistent, non‐inactivating Na⁺ current and [Ca²⁺]_i regulation in CA1 pyramidal cells. The described cellular mechanisms are most likely part of the pathomechanism of certain forms of epilepsy that are associated with I_Na,P. Describing the magnitude, temporal pattern and sources of Ca²⁺ increase induced by I_Na,P may provide novel targets for antiepileptic drug therapy.     

Transformation of Pasteurella novicida

Deoxyribonucleic acid from a streptomycin-resistant mutant of Pasteurella novicida transformed portions of P. novicida streptomycin-sensitive populations to streptomycin-resistant. Similarly, mutants auxotrophic for tryptophan or purine biosynthesis were also transformed to nutritional independence.     

Repair of psoralen and acetylaminofluorene DNA adducts by ABC excinuclease

Escherichia coli UvrA, UvrB and UvrC proteins acting in concert remove the major ultraviolet light-induced photoproduct, the pyrimidine dimer, from DNA in the form of a 12 to 13-nucleotide long single-stranded fragment. In vivo data indicate that the UvrABC enzyme is also capable of removing other nucleotide diadducts as well as certain nucleotide monoadducts from DNA and initiating the repair process that leads to removal of interstrand crosslinks caused by some bifunctional chemical agents. We have determined the action mechanism of the enzyme on nucleotide monoadducts produced by 4'-hydroxymethyl-4,5',8-trimethylpsoralen and N-acetoxy-N-2-acetylaminofluorene. In both cases we find that the enzyme hydrolyzes the eighth phosphodiester bond 5' and the fifth phosphodiester bond 3' to the modified base. This cutting pattern is similar to that observed with diadduct substrate, the only difference being that while the enzyme incises the fourth or fifth phosphodiester bond 3' to the pyrimidine dimer it always hydrolyzes the fifth bond relative to monoadducts. Our results also suggest that ABC excinuclease cuts the same two phosphodiester bonds on both sides of a T whether that T has a psoralen monoadduct or is involved in psoralen-mediated interstrand crosslink.