Influence of systemic copper toxicity on early development and metamorphosis in Xenopus laevis.

The primary objective of the present study was to examine the influence of early systemic toxicity resulting from copper (Cu) exposure on metamorphic processes in Xenopus laevis. A 28-day exposure study with copper, initiated at developmental stage 10, was performed using test concentrations of 3.0, 9.0, 27.2, 82.5, and 250 µg Cu/L. The primary endpoints included mortality, developmental stage, embryo-larval malformation, behavioral effects, hindlimb length (HLL), growth (snout-vent length [SVL] and wet body weight), and histopathology. The 28-day LC50 value with 95% confidence intervals was 61.2 (51.4-72.9) µg Cu/L with 250 µg Cu/L resulting in complete lethality. Developmental arrest in the 82.5 and delay in the 27.2 µg Cu/L treatments was observed as early as study day 10 continuing throughout the remainder of exposure. SVL-normalized HLL, body weight, and SVL in the 27.2 and 82.5 µg Cu/L treatments were significantly decreased relative to control. At 82.5 µg Cu/L, and thyroid gland size was markedly reduced when compared with controls consistent with the stage of developmental and growth arrest. Concentration-dependent findings in the intestine, liver, gills, eyes, and pharyngeal mucosa were consistent with non-endocrine systemic toxicity. These were prevalent in the 9.0 and 27.2 µg Cu/L treatment groups but were minimally evident or absent in the 82.5 µg/L group, which was attributed to developmental arrest. In conclusion, developmental delay in larvae exposed to 27.2 and 82.5 µg Cu/L was the result of systemic toxicity occurring in early development prior hypothalomo-pituitary-thyroid axis (HPT)-driven metamorphosis and was not indicative of endocrine disruption.

Importance of diet in amphibian metamorphosis-based studies designed to assess the risk of thyroid active substances.

The present study evaluated the hypothesis that dietary quality used in historical studies may impact the effects of chemical stressors on premetamorphic development and metamorphosis due to suboptimal nutritional quality. A modified Amphibian Metamorphosis Assay (AMA) was performed in which Nieuwkoop and Faber (NF) Stage 47 tadpoles of Xenopus laevis were exposed for 32 days to iodide (I- )-deficient FETAX solution supplemented with <0.025, 0.17, 0.52, 1.58, and 4.80 µg I- /L (measured concentrations 0.061, 0.220, 0.614, 1.65, and 4.73 µg I- /L) and fed a pureed Frog Brittle (FB) diet. An AMA guideline benchmark group (four replicates) exposed to dechlorinated tap water and fed standard Sera Micron Nature® (SMN) diet was evaluated concurrently. Developmental delay, observed as changes in stage distribution or median developmental stage, occurred in FB treatments with 0.061, 0.220, and 0.614 µg/L I- , respectively. Developmental rates and hind limb length of the 1.65 and 4.73 µg/L I- groups were similar to each other, but both treatments fell short of the developmental rate achieved by the SMN benchmark. Iodide supplementation also had no impact on nonthyroidal growth endpoints, which were markedly reduced in FB-fed frogs compared with their SMN-fed counterparts. All larvae that received the FB diet had mildly to severely hypoplastic/atrophic thyroids, a condition for which iodine supplementation had little if any ameliorative effect. Collectively, these results suggested that nutritional deficiencies in the FB diet negatively affected both growth and metamorphic development, the latter of which was only compensated to a limited extent by iodine supplementation.

Toxicity of sulfide to early life stages of wild rice (Zizania palustris).

The sensitivity of wild rice (Zizania palustris) to sulfide is not well understood. Because sulfate in surface waters is reduced to sulfide by anaerobic bacteria in sediments and historical information indicated that 10 mg/L sulfate in Minnesota (USA) surface water reduced Z. palustris abundance, the Minnesota Pollution Control Agency established 10 mg/L sulfate as a water quality criterion in 1973. A 21-d daily-renewal hydroponic study was conducted to evaluate sulfide toxicity to wild rice and the potential mitigation of sulfide toxicity by iron (Fe). The hydroponic design used hypoxic test media for seed and root exposure and aerobic headspace for the vegetative portion of the plant. Test concentrations were 0.3, 1.6, 3.1, 7.8, and 12.5 mg/L sulfide in test media with 0.8, 2.8, and 10.8 mg/L total Fe used to evaluate the impact of iron on sulfide toxicity. Visual assessments (i.e., no plants harvested) of seed activation, mesocotyl emergence, seedling survival, and phytoxicity were conducted 10 d after dark-phase exposure. Each treatment was also evaluated for time to 30% emergence (ET30), total plant biomass, root and shoot lengths, and signs of phytotoxicity at study conclusion (21 d). The results indicate that exposure of developing wild rice to sulfide at ≥3.1 mg sulfide/L in the presence of 0.8 mg/L Fe reduced mesocotyl emergence. Sulfide toxicity was mitigated by the addition of Fe at 2.8 mg/L and 10.8 mg/L relative to the control value of 0.8 mg Fe/L, demonstrating the importance of iron in mitigating sulfide toxicity to wild rice. Ultimately, determination of site-specific sulfate criteria taking into account factors that alter toxicity, including sediment Fe and organic carbon, are necessary. Environ Toxicol Chem 2017;36:2217-2226. © 2017 SETAC.