Natural organic matter (NOM) was concentrated from various sites across Canada using a portable reverse-osmosis unit to obtain a range of NOM types, from mainly allochthonous (terrestrially derived) to mainly autochthonous (aquatically derived) NOM. The addition of NOM to Cu exposures in ion-poor water always decreased Cu toxicity to rainbow trout (Oncorhynchus mykiss, approximately 1 g) over a 96-h period, and the degree of protection varied with respect to NOM source. A good correlation was found between the specific absorbance coefficient (SAC) and time to reach 50% mortality (LT50; p < 0.001), indicating that more optically dark, allochthonous-like NOM decreases Cu toxicity better than does optically light, more autochthonous-like NOM. A similar, good relationship between NOM source and Pb toxicity was seen (p < 0.001), once confounding effects of Ca binding to NOM were accounted for. No significant relationship between Cd toxicity and NOM optical quality was seen (p = 0.082), and in toxicity tests with Cd the presence of some of the NOM sources increased Cd toxicity compared to Cd-only controls. Specific absorbance coefficients were used as a proxy measurement of NOM aromaticity in our study, and fluorescence indices were run on some NOM samples to obtain percent aromaticity for each sample. A good correlation was found between SAC and percent aromaticity, indicating that the simple SAC measurement is a reasonable indication of NOM aromaticity and of metal binding by NOM.

No abstract

The developing female sheep, which attains puberty after 25 weeks of age, was used as an experimental model to investigate the role of endogenous opioid peptides in the control of pulsatile LH secretion during sexual maturation. Treatment of ovary-intact prepubertal sheep at 12 weeks of age with the opiate antagonist naloxone resulted in a dose-dependent increase in LH secretion. Subsequent studies used ovariectomized (OVX) lambs implanted with capsules containing 17 beta-estradiol to provide a constant, ovarian steroid feedback signal throughout development. Naloxone treatment (hourly iv injections of 1 mg/kg BW for 4 h) produced an increase in the frequency of episodic LH secretion at all prepubertal ages, when lambs were highly sensitive to the estradiol negative feedback. However, increases in LH pulse frequency were also induced by naloxone treatment at a postpubertal age in estradiol-treated OVX sheep, indicating that opioid inhibition is still present at a time when sensitivity to the feedback effects of ovarian steroids is markedly reduced and endogenous LH secretion is increased. These observations in ovary-intact and estradiol-treated OVX lambs suggest that opioid mechanisms inhibit pulsatile tonic LH secretion during both the prepubertal and postpubertal periods. Endogenous opioid inhibition of LH secretion is not dependent on the presence of ovarian steroids, as evidenced by the response to naloxone 3 weeks after removal of an estradiol implant from OVX lambs, when LH pulse frequency was already high. Naloxone treatment increased LH pulse frequency further, at both a prepubertal age (18 weeks) and a postpubertal age (38 weeks). Naloxone also increased LH pulse frequency in OVX lambs in which LH secretion was inhibited chronically by progesterone rather than by estradiol. The response to naloxone was similar in postpubertal P-treated OVX lambs and age-matched prepubertal P-treated OVX controls in which puberty had been delayed by means of an inhibitory seasonal photoperiod. In addition, after removal of steroid implants to allow LH secretion to increase, the degree of inhibition of LH secretion by the opiate agonist morphine was similar between age-matched postpubertal sheep and those with photoperiodically delayed puberty. We conclude that endogenous opioid mechanisms are an important inhibitory mechanism controlling pulsatile LH secretion in the developing sheep. However, changes in opioid inhibition are unlikely to underlie the decrease in sensitivity to steroid negative feedback and increase in pulsatile LH secretion that occur at puberty.

No abstract

Rainbow trout (Oncorhynchus mykiss; 2-17 g) were exposed to approximately 0.1 microM silver as AgNO3 for 3 to 4 h in synthetic, ion-poor water (20 microM Ca, 100 microM Na, 150 microM Cl, pH 7) to which was added Mg, Ca, or thiosulfate (S2O3). Gills were extracted and assayed for Ag using graphite furnace atomic absorption spectrophotometry. Up to 210 mM Mg (fourfold the concentration of Mg in seawater) did not reduce accumulation of Ag by trout gills. The conditional equilibrium stability constant (K) for Mg at silver-binding sites on the gills was calculated to be log K(Mg-gillAg) = 3.0, or approximately half-as-strong binding as for Ca at these sites. The inclusion of the Mg-gill stability constant into the original Ag-gill binding model increases the flexibility of the model, although the competitive effects of Mg are only important in sodium-poor systems.