Benzene-assisted atmospheric-pressure chemical ionization: a new liquid chromatography/mass spectrometry approach to the analysis of selected hydrophobic compounds.

Charge-exchange reactions involving benzene have been successfully exploited to increase the sensitivity of atmospheric-pressure chemical ionization mass spectrometry (APCI-MS) towards hydrophobic compounds of significant environmental relevance which are not detectable with the ordinary APCI techniques. Among them, good sensitivity have been found for (a) highly chlorinated biphenyl derivatives such as dichlorodiphenyltrichloroethane (DDT), dichlorodiphenyldichloroethane (DDD) and dichlorodiphenyldichloroethene (DDE); (b) cyclopentadienes such as Aldrin and its epoxy derivatives Dieldrin and Endrin; and (c) dibenzofurans and dibenzo-para-dioxins such as 2,3,7,8-tetrachlorodibenzofuran (2,3,7,8-TCDF) and 2,3,7,8-tetrachloro-dibenzo-para-dioxin (2,3,7,8-TCDD). The reactant benzene molecules were introduced into the source either through the nebulizer gas or by direct post-column addition of neat liquid, whereas the targeted compounds were analyzed using a high-performance liquid chromatography (HPLC) RP-18 column using methanol/water solutions as mobile phase. By using benzene as post-column reagent, positive ion mode detection was proven to be significantly enhanced as compared with APCI measurements carried out without benzene assistance.

Toxicological significance of dihydrodiol metabolites.

Dihydrodiols are often found as the major organic-extractable metabolites of various olefinic or aromatic xenobiotics in many biological samples. Studies on the chemistry of dihydrodiol metabolites have provided insight into the pharmacokinetic behavior and the mode of action of the parent compound. The toxicology of dihydrodiol is more complex than what can be deduced solely on the basis of diminished bioavailability of the epoxide precursor, and the increased hydrophilicity associated with the dihydrodiol moiety. Dihydrodiols can be intrinsically toxic and may even represent metabolically activated species. Some of the dihydrodiol metabolites may still retain sufficient lipophilic character to serve again as substrates for microsomal oxygenases. Because of the tremendous chemical and biological diversity that existed among the various dihydrodiols, more mechanistic studies are needed to examine the toxicological properties of these compounds. It may be premature to conclude dihydrodiol formation as purely a detoxification route for xenobioties.

Fate of [14C]aldrin in crop rotation under outdoor conditions.

[14C]Aldrin was applied to soils (about 3kg/ha) in outdoor boxes at various locations (Germany, England, and United States), and crops were cultivated (maize, wheat, sugar beets, and potatoes). In the following year, crop rotation experiments were carried out in the same soils without retreatment; in addition, wheat was grown in soils retreated with [14C]aldrin (3.5 kg/ha). After the harvest of both years, the distribution of aldrin and major metabolites (dieldrin; photodieldrin; hydrophilic metabolites including dihydrochlordene dicarboxylic acid; an unidentified nonpolar compound X; and unextractable metabolites) was determined in plants, soils, and leaching water. Two further conversion products, photoaldrin and aldrin-trans-diol, occurred in trace amounts only in a few samples. Metabolic pathways for aldrin under outdoor conditions are presented. The distribution of radioactive residues in soils and plants as well as their quantitative chemical composition are discussed, and comparisons are made between the different experimental sites, the crops, the first and second year, and retreated and nonretreated samples. The quantitative results are compared to those of field trials.

Excitatory and depressant effects of dieldrin and aldrin-transdiol in the spinal cord of the toad (Xenopus laevis).

An investigation was made into the action of the insecticide dieldrin and one of its metabolites, aldrin-transdio, on the isolated spinal cord of the toad, Xenopus laevis. Conventional electrophysiological techniques were used for stimulating and recording of dorsal and ventral spinal roots. An augmentation of polysynaptic reflex activity along with a marked reduction of orthodromic postsynaptic inhibition could be demonstrated in preparations isolated from dieldrin-poisoned animals. However, application of dieldrin to the isolated spinal cord failed to produce any significant effect. Application of aldrin-transdiol, on the other hand, caused a potentiation of spinal reflex activity and an increase in spontaneous activity of ventral and dorsal roots. Aldrin-transdiol also produced a marked reduction of spinal inhibitory mechanisms. The excitatory effects of aldrin-transdiol were followed by a strong depressant action on spinal excitability.

Effects of aldrin-transdiol on neuromuscular facilitation and depression.

The effects of aldrin-transdiol, one of the active metabolites of the insecticide dieldrin, on evoked transmitter release, neuromuscular facilitation and neuromuscular depression have been studied in frog sartorius nerve-muscle preparations. Conventional techniques of intracellular recordings were used. Aldrin-transdiol caused a marked increase in end-plate potential amplitude under conditions of low quantal content, i.e., in Mg2+-blocked junctions. The increase in end-plate potential amplitude was less pronounced in curarized junctions, in which the transmitter release was not impaired. Concomitant with the increase in end-plate potential size there was a marked enhancement of facilitation during short trains of stimuli applied to the motor nerve. The decay of facilitation was, however, not seriously affected by aldrin-transdiol. These effects may be explained in terms of the known 'calcium hypothesis' by assuring that aldrin-transdiol increases the amount of calcium which enters the nerve terminal during the nerve impulse. The increase in end-plate potential amplitude and in facilitation by aldrin-transdiol was transient. At later stages of poisoning, end-plate potential and facilitation decreased below control level and neuromuscular depression was significantly enhanced. This latter effect may be the result of a direct inhibitory effect of aldrin-transdiol on transmitter mobilization. As far as the fall in end-plate potential amplitude is concerned the known suppressive action of aldrin-transdiol on the chemical sensitivity of the postsynaptic membrane and on the nerve action potential probably plays a part as well. Finally, neuromuscular transmission was completely blocked by aldrin-transdiol.