Detecting a field gradient of PAH exposure in decapod crustacea using a novel urinary biomarker.

Norwegian coastal waters are subject to PAH contamination from electrochemical industries such as aluminium smelters. Evidence of PAH exposure has been established in fish and bivalves. The present study tests the applicability of a novel crustacean PAH exposure biomarker to a PAH contamination gradient in the field (Karmsund Strait, SW Norway). Fluorescence analysis of urine samples collected from crabs at each site revealed 1-OH pyrene "equivalent" levels (indicative of pyrogenic PAH contamination) decreased with increasing distance from a point source of pyrogenic PAH (a large aluminium works). The assay was shown to be suitable for the detection of PAH exposure in wild crustacean populations, for discriminating between contaminated and clean sites and is also sufficiently sensitive to detect gradients of PAH contamination. The method provides a rapid, inexpensive and non-destructive measure of biologically available PAH in crustaceans.

Biochemical and histological responses in mussel (Mytilus edulis) exposed to North Sea oil and to a mixture of North Sea oil and alkylphenols.

Several environmental chemicals are suspected to be responsible for adverse health effects on the reproductive system in various organisms. During this work, environmentally relevant concentrations of North Sea oil were used alone or in combination with alkylphenols and additional PAH to study the effect on vitellogenin-like protein expression and gonadal development in mussels. North Sea oil (0.5 ppm) induced the expression of phospho-proteins in both sexes indicating that some compounds are oestrogen-mimics. This induction was not seen in samples dosed with the mixture but signs of toxic effects were observed in the gonads. Indeed, numerous degenerating ovarian follicles in females and foci, similar to vertebrate melanomacrophage centres, were observed in testes.

Effects of an opioid antagonist on pain intensity and withdrawal reflexes during induction of hypnotic analgesia in high- and low-hypnotizable volunteers.

The aim of this investigation was to study the effect of suggestions of hypnotic analgesia on spinal pain transmission and processing. Pain intensity and amplitude of nociceptive withdrawal reflexes to electrical stimuli were measured in 10 high- and 10 low-hypnotizable subjects during two sessions taking place at least 24 h apart under five conditions of: (1) pre-hypnosis; (2) neutral hypnotic relaxation; (3) suggestions of hypnotic analgesia; (4) suggestions of hypnotic analgesia after injections of either naloxone (1 ml, 1 mg/ml) or saline (1 ml) under double-blinded conditions; and (5) post-hypnosis. The conditions of naloxone or saline were allocated at random to either Day 1 or Day 2 in a double-blinded fashion. Results showed significant reductions of pain intensity during hypnotic analgesia, and a significant reduction in nociceptive reflexes during hypnotic analgesia on Day 1 in the highly hypnotizable group. No differences were found for low-hypnotizable subjects. The results support previous findings that pain intensity as well as the nociceptive reflex can be modulated by suggestions of hypnotic analgesia. While no effect of naloxone on pain intensity was found during hypnotic analgesia, naloxone significantly reversed the suppressive effect of suggestions of hypnotic analgesia on reflexes in high-hypnotizable subjects. Subsequent analysis showed that the effect of naloxone was associated with the intensity of the stimulus needed to elicit a reflex, and was unrelated to hypnotic susceptibility when controlling for stimulus intensity. These results suggest that the effect of naloxone was related to the greater stimulus intensities needed to elicit a reflex in the high-hypnotizable group, rather than to hypnosis or hypnotic susceptibility in itself. It is unclear why greater stimulus intensities were needed in high-hypnotizable subjects and further studies are needed. Copyright 1998 European Federation of Chapters of the International Association for the Study of Pain.