Morphological indices and otolith microstructure of Atlantic croaker,Micropogonias undulatus,as indicators of habitat quality along an estuarine pollution gradient

Synopsis Atlantic croaker, Micropogonias undulatus, sampled from a transect along a pollution gradient show a trend of declining growth and physical condition. This trend is apparent in the mean size of 0-group croaker, in their recent growth rate measured by marginal otolith increment widths, in longer term growth rate as indicated by relative otolith weights, and in general physical condition as measured by an index of condition of the caudal fin. We suggest that these measures are indicators of stress associated with environmental conditions. Because croaker from different positions along the pollution gradient were distinguishable, it appears that they remain for extended periods within areas of degraded environmental quality.     

Genetic and Structural Analysis of Five Arabidopsis Mutants with Abnormal Root Morphology Generated by the Seed Transformation Method

A number of Arabidopsis thaliana mutants with abnormal rootmorphology have been isolated from a population of Agrobacterium-mediated seed transformants. Five of these mutants identifiedby their abnormal root morphology have been genetically andmorphologically characterised. Two mutants, 5905 and 1767 havedefective cellular elongation, mutant 7203 lacks an endodermalcell layer and mutants 4792 and 7133 exhibit abnormal radialcellular expansion. It is apparent from detailed analysis thatabnormal root morphology is accompanied by abnormal hypocotylphenotype. Genetic analysis has revealed that only one of thesemutants is tagged with a T-DNA insert.Copyright 1994, 1999 AcademicPress Arabidopsis thaliana, root, development, T-DNA insertion mutagenesis, endodermis, elongation     

Effects of diethyldithiocarbamate (ddtc) on the plasma biotransformations of tetrachloro(d,i-trans)-1,2-diaminocyclohexaneplatinum(iv) (tetraplatin) in fischer 344 rats

We have studied the effects of diethyldithiocarbamate (DDTC) on the biotransformations of toxic doses of tetrachloro (d,l-trans)1,2-diaminocyclohexaneplatinum(IV) (tetraplatin) in Fischer 344 rats. In animals not treated with DDTC, tetraplatin was rapidly converted to dichloro(d,I-trans)1,2-diaminocyclohexaneplatinum(II) [PtCl₂(dach]. Subsequent biotransformations included the transient formation of the (d,I-trans)1,2-diaminocyclohexane-aquachloroplatinum(II) [Pt(H₂O)(Cl)(dach)]+ complex, followed by formation of the platinum (Pt)-methionine and either Pt-cysteine or Pt-ornithine complexes. Significant amounts of free (d,I-trans) 1,2-diaminocyclohexane (dach) were observed in plasma as a result of intracellular trans-labilization reactions. DDTC caused a marked decrease in both total and protein-bound platinum in the circulation. A significant increase in the plasma concentration of free dach was also observed as a result of formation of the Pt(DDTC)₂ complex. Some of the free dach could have arisen from intracellular reactions with DDTC, but the displacement of platinum from plasma proteins was more than sufficient to account for the increase in free dach in the circulation. DDTC treatment also decreased plasma concentrations of tetraplatin, PtCl₂(dach), [Pt(H₂O)(Cl)(dach)]⁺, the Pt-methionine complex, and one unidentified biotransformation product, but had no effect on the Pt-cysteine (or Pt-ornithine) complex. These effects of DDTC on protein-bound platinum and low-molecular-weight biotransformation products in plasma may contribute to the decrease in tetraplatin toxicity seen in DDTC-treated rats.     

Reperfusion-induced arrhythmias are not prevented by ibuprofen in isolated rat heart

Free radicals have been implicated in the genesis of reperfusion-induced arrhythmias and the cyclooxygenase pathways has been suggested as a potential source. We have therefore assessed whether a cyclooxygenase inhibitor, ibuprofen, is able to reduce reperfusion-induced injury in the isolated perfused rat heart. A duration of 10 min of regional ischemia, which resulted in a high (83%) incidence of ventricular fibrillation, was selected and hearts (n = 12/group) were perfused with ibuprofen (2, 20, or 30 mg/L) throughout the experiment. Ibuprofen did not affect heart rate, although it did produce a dose-dependent increase in coronary flow. However, at all doses studied, ibuprofen had no effect upon the time to onset, incidence, or duration of arrhythmias. In subsequent studies with 30 min of regional ischemia, ibuprofen (30 mg/L) again caused vasodilatation but without effect upon heart rate or severity of arrhythmias. In conclusion, we were unable to obtain evidence in support of the concept that cyclooxygenase activity or cyclooxygenase-derived free radicals are involved in the genesis of ischemia- and reperfusion-induced arrhythmias.