Delayed effects of embryonic exposure of zebrafish (Danio rerio) to methylmercury (MeHg).

Since previous short-term bioassays of methylmercury (MeHg) indicated no morphological effects in zebrafish (Danio rerio) after embryonic exposures below 20 microg/l MeHg, studies were done to determine whether embryonic exposure to MeHg at lower concentrations would induce behavioral effects. Newly fertilized embryos were exposed to 0, 5, 10 or 15 microg MeHg/l for selected exposure durations: single day, multiple day or continuous exposure from fertilization through hatching. Larvae were maintained in an essential salt solution after hatching. Spontaneous swimming performance and prey capture experiments were conducted. Continuous embryonic exposure to 15 microg/l caused delayed mortality syndrome (DMS). These larvae hatched normally and appeared normal, but beginning at Day 3 post-hatch (ph), general activity was severely reduced and by Day 5 ph, larvae were completely moribund; many had faint heartbeats, severely enlarged body cavities and upward flexures of the spinal cord. Most of these larvae were dead by Day 6 ph. Multi- and single-day embryonic exposures to 15 microg/l caused reduced swimming activity and prey capture ability, and by Day 4 ph, these larvae also began to show signs of DMS. Continuous embryonic exposure to 10 microg/l significantly reduced spontaneous swimming activity, which did not improve after 5 days in clean water. Similar results were seen in larvae exposed during the last 24 h of embryonic development. Prey capture ability was also impaired in larvae exposed continuously to 10 microg/l, even after 4 days in clean water. Single-day exposures to 10 microg/l did not affect prey capture ability. Larvae from the 5-microg/l exposures were not significantly different from controls for either parameter. This study reinforces the idea that functional impairment is a more subtle response to developmental toxicants than mortality or the production of morphological defects.

Intraarticular sodium hyaluronate injections in the Pond-Nuki experimental model of osteoarthritis in dogs. I. Biochemical results.

An established anterior cruciate ligament deficiency-induced articular cartilage degeneration was used to evaluate the effects of intrasynovial injection of hyaluronic acid upon cartilage destruction. In this study, proteoglycan solubility under associative and dissociative conditions was compared in two treatment protocols at intervals of seven, 13, and 17 weeks after surgical breakage of the anterior cruciate ligament in 2.5-year-old Beagle dogs. Untreated joints showed a marked increase in both total soluble glycosaminoglycan (GAG measured as uronic acid) and in the associative fraction. In both treated groups, there was a reduced amount of soluble GAG. Cessation of treatment after seven weeks caused gradual regression, with an increasing amount of CaCl2-soluble material in the associative fraction, while inception at seven weeks gave biochemical evidence of reversal, with increasing GAG present in the guanidine-soluble (dissociative) fraction on the insoluble residue. The protective effects of hyaluronic acid suggest the potential clinical application of this therapy in retarding the advance of osteoarthritis.