Nickel toxicity in embryos and larvae of the South American toad: effects on cell differentiation, morphogenesis, and oxygen consumption.

Nickel, a widely distributed heavy metal in the biosphere, produces systemic, carcinogenic, and teratogenic effects. The objectives of the present study are to report the acute, short-term chronic, and chronic toxicity of Ni in Rhinella arenarum embryos as well as the stage-dependent susceptibility to this heavy metal, including oxygen consumption, teratogenesis, and adverse effects on cell differentiation processes. The stages evaluated were blastula (S.7), gastrula (S.11), tail bud (S.17), fin circulation (S.22), and complete operculum (S.25), in this last case by means of toxicity profile curves. Nickel increases its adverse effects gradually, with a maximum value after 96 h. The 50% lethal concentrations (LC50s) for 96, 168, and 240 h at S.25 were 1.14, 0.60, and 0.48 mg Ni²(+) /L, respectively; S.11 and S.22 were the least and most susceptible to Ni with, LC50s 96 h of 6.12 and 0.19 mg Ni²(+) /L, respectively. A reduction of approximately 25% in oxygen consumption anticipates lethal effects from S.17 onward. The main teratogenic effects were retarded growth and development, extremely severe axis incurvations, persistent yolk plug, asymmetry, microcephaly and mouth and gill agenesia, and limited neuromuscular activity. Ciliated cells were not functional. The possibility of associating the remarkable stage-dependent susceptibility to Ni with environmental changes during the evolutionary process is also considered.

Acute and subchronic toxicity of arsenite and zinc to tadpoles of Rhinella arenarum both alone and in combination.

The current study evaluated acute and subchronic toxicity of arsenite (As(3+)) and zinc (Zn(2+)) to stage 25 tadpoles of Rhinella arenarum in both single and joint laboratory exposures. LC50 values obtained for As(3+) were elevated and remained within the range of 46 to 50 mg/L of As(3+) between 4 and 17 d of exposure. Growth of tadpoles was completely inhibited with 30 mg/L of As(3+), demonstrating the presence of ecologically relevant sublethal effects at concentrations lower than those resulting in lethality. With respect to Zn(2+), a 96-h LC50 value of 2.49 mg/L was calculated in soft water. Contrary to results obtained for As(3+), LC50 values of Zn(2+) gradually decreased with increasing exposure duration, from 2.49 mg/L at 96 h to 1.30 mg/L after 21 d. In joint exposures to both metals, the type of interaction observed between As(3+) and Zn(2+) was concentration dependent. Lethal effects of As(3+) were mitigated, unaffected, or potentiated by 0.01, 0.1, and 1-2 mg/L of Zn(2+), respectively. However, although 0.01 mg/L of Zn(2+) significantly reduced lethality of As(3+)-exposed tadpoles, the same concentration of Zn(2+) did not help to reverse the stunt growth of these animals. Further studies need to examine which are the lowest concentrations As(3+) required to reduce growth and whether Zn(2+) serves to antagonize growth effects in this range of concentrations.

Nickel tissue residue as a biomarker of sub-toxic exposure and susceptibility in amphibian embryos.

Although low level exposure to physicochemical agents is the most common environmental scenario, their effects on living organisms are very controversial. However, there is an increasing need to integrate low level exposures from risk assessment to remediation purposes. This study focus on the possibility to employ Ni tissue residue values as biomarkers of sub-toxic exposure and susceptibility to this metal in a range of almost pristine to sub-toxic concentrations for Rhinella arenarum embryos. For that purpose, three batches of amphibian embryos were pretreated during 10 days with three increasing concentrations of Ni starting in 2, 8 and 20 microg Ni(2+) L(-1) and ending in 16, 64 and 160 microg Ni(2+) L(-1) (in natural fresh waters this value ranges from 2 to 10 microgL(-1); the LC(50)-24h for R. arenarum is 26.2mg Ni(2+) L(-1)). For the experimental conditions, the Ni tissue residue values at 360 h post exposure were 0.5, 2.1 and 3.6 microg Ni g(-1) embryo w/w, respectively, corresponding to BCFs of 31, 33 and 23. The susceptibility to Ni in those experimental embryos was evaluated by means of challenge exposures to three lethal concentrations of this metal (10, 20 and 30 mg Ni(2+) L(-1)), registering survival during the following 10 days of treatment. As a general pattern, the lower, intermediate and higher pretreatments with Ni resulted in enhanced, neutral and adverse effects on embryonic survival, respectively. Thus, sub-toxic exposure to Ni could modify the resistance of the amphibian embryo to this metal and Ni tissue residue values could be considered as biomarkers of both, exposure and susceptibility.