Living organisms influence on environmental conditions: pH modulation by amphibian embryos versus aluminum toxicity.

The LC10, 50 and 90/24h of aluminum for Rhinella arenarum embryos at complete operculum stage were 0.55, 0.75 and 1mgAl(3+)/L respectively. Those values did not change significantly by expanding the exposure period till 168h. The aluminum toxicity was evaluated in different pH conditions by means of a citrate buffer resulting for instance, 1mgAl(3+)/L at pH 4, 4.1, 5 and 6 in 100%, 70%, 35% and 0% of lethality respectively. As an outstanding feature, the embryos changed the pH of the maintaining media both in the case of Al(3+) or citrate buffer treatments toward neutral. 10 embryos in 40mL of AMPHITOX solution were able to increase the pH from 4.2 to 7.05, a fact related with a metabolic shift resulting in an increase in nitrogen loss as ammonia. Our study point out the natural selection of the most resistant amphibian embryos both for pH or aluminum as well as the capacity of living organisms (as a population) to alter their chemical environment toward optimal conditions for their survival. As these facts occur at early life stages, it expand the concept that living organisms at ontogenic stages are biomarker of environmental signatures of the evolutionary process (Herkovits, 2006) to a global Onto-Evo concept which imply also the feedback mechanisms from living organisms to shape environmental conditions in a way that benefits them.

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.