ABSTRACT
Isotherapics preparedfromtoxic substances have been described as attenuation factors for heavy metal intoxicationin aquatic animals. Herein, Artemia salinaand mercury chloride were usedas a model to identify treatment-related bioresilience. The aim was to describe the effects of Mercurius corrosivus(MC) in different potencies on Artemia salinacyst hatching and on mercury bioavailability. Artemia salinacysts were exposed to 5.0 µg/mL of mercury chloride during the hatching phase. MC6cH, 30cH, and 200cHwere prepared and poured into artificial seawater. Different controls were used (nonchallenged cysts and challenged cysts treated with water, succussed water, and Ethilicum 1cH). Four series of nine experiments were performed for4 weeks to evaluate the percentage of cyst hatchingconsidering all moon phases. Soluble total mercury (THg) levels and precipitated mercury content were also evaluated. Solvatochromic dyes were used to check for eventual physicochemical markers of MCbiological activity. Two-way analysis of variance (ANOVA) with mixed modelswas used for evaluating the effect of different treatments andthe simultaneous influence of the moon phases on the cystshatching rate, at both observation times (24 and 48 hours).When necessary, outliers were removed, using the Tukeycriterion.Thelevel of significance αwas set at 5%. Significant delay (p<0.0001) in cyst hatching was observed after treatment with MC30cH, compared with the controls. An increase inTHg concentration in seawater (p<0.0018) and of chlorine/oxygen ratio (p<0.0001) in suspended micro-aggregateswas also seen, with possiblerelation with mercury bioavailability. Specific interaction of MC30cH with the solvatochromic dye ET33 (p<0.0017) was found. The other observed potencies of Mercurius corrosivus6 and 200 cH were not significant in relation to the observed groups.The results werepostulated as being protective effects of MC30cH on Artemia salina, by improving its bioresilience.
Subject(s)
Artemia , Ecotoxicology , Homeopathy , MercuryABSTRACT
Nos anos de 2001 e 2002, 46 cabritos (CAB) e 35 cordeiros (COR) de uma propriedade do agreste do Estado de Pernambuco foram acometidos por ataxia enzoótica (AE) de forma tardia. Houve aumento da incidência do 1o ano (46,3 por cento - CAB; 24,2 por cento COR) para o ano subseqüente (100 por cento - CAB e COR). Somente no ano de 2001, houve maior incidência em CAB (P<0,002) que nos COR. Todos os animais acometidos sucumbiram, com exceção de um CAB e um de COR. O quadro clínico variou de acordo com a idade em que surgiram os sintomas, ou seja, de 30 a 45 dias os animais manifestaram paralisia dos membros anteriores e posteriores, acompanhada de espasticidade muscular e morte; com mais de 45 dias, ocorreu paralisia flácida ou espástica apenas dos membros posteriores e morte; somente os cabritos com menos de 45 dias apresentaram movimentos verticais de cabeça. As lesões histopatológicas evidenciadas foram: degeneração axonal, esferóides, gliose e dismielinização no segmento ventral e lateral da medula espinhal. Nos animais com menos de 45 dias, essas lesões foram evidentes na região cervical e nos animas mais velhos na região lombar. Apenas nos cabritos foi constatada lesão degenerativa no cerebelo. A dieta oferecida ao rebanho continha quantidades adequadas de cobre, porém os animais acometidos por AE apresentaram baixos teores de cobre no fígado (45,8mg kg-1 MS). Os elementos antagonizantes do cobre, Mo, S, e Zn, estavam normais, com exceção do ferro, que estava em alta concentração tanto no solo (8600mg kg-1) quanto nos alimentos (284mg kg-1). O excesso de ingestão de ferro sugere ter provocado a carência de cobre nos animais.