Abstract
Chickens were fed alkyl mercury-dressed wheat (mercury content about 8 mg/kg) for 35–44 days and were then immediately sacrificed. No signs of untoward effects were observed. Muscle of the chickens, and a minor proportion of liver, were fed to two groups of two ferrets (Mustela furo L. × M. putorius L.), the mercury content of the diet being 7 and 5 mg/kg, respectively. The ferrets of the first group died after 35 and 36 days and those of the second after 58 days.
The experimental ferrets showed a marked weight loss, attributable to muscular atrophy in addition to a reduced food intake. Clinical signs appeared in two to three weeks and were primarily neurological such as ataxia, trembling and paralysis. The signs could be correlated with pronounced degenerative changes of the central and peripheral nervous systems involving mainly the cerebellum and peripheral nerves and, to a lesser extent, the cerebrum and the spinal cord. Hypoplasia of the lymphatic tissue of the spleen and degeneration of the graafian follicles were seen as well.
High mercury levels were found in the kidneys, liver and brain and also in skeletal muscle and the gonads of the ferrets (Table 2). Methyl mercury constituted the major part of the tissue mercury in the ferrets (as well as in the chickens).
The results provide direct evidence of the transfer and accumulation of alkyl mercury in a toxic form through a food chain. The ecological implications are discussed.
Sammanfattning
Tamhöns utfodrades med alkylkvicksilverbetat vete (kvicksilverhalt ca. 8 mg/kg) under 35—44 dagar och avlivades omedelbart därefter. Inga tecken på förgiftning iakttogs.
Två grupper (vardera på 2 djur) av iller utfodrades med muskulatur (och en ringa tillblandning av lever) från hönsen. Den genomsnittliga kvicksilverhalten i fodret hos de två grupperna var 7 resp 5 mg/kg. Djuren i den första gruppen dog efter 35 och 36 dagar och de i den andre efter 58 dagar.
En påtaglig viktsförlust noterades hos försöksillrarna, vilken kunde tillskrivas skelettmuskelatrofi i förening med nedsatt foderintag. I övrigt iakttogs, med början efter 2—3 veckor, huvudsakligen förgiftningssymptom av neurologisk art, såsom ataxi, darrningar och förlamningar. Symtomen kunde korreleras med degenerativa förändringar främst i lillhjärna och perifera nerver men även i storhjärna och ryggmärg. Därjämte iakttogs hypoplasi av mjältens lymfatiska vävnad och follikeldegeneration i ovarierna.
Höga kvicksilverhalter påvisades i njurar, lever och hjärna och även i skelettmuskulatur och gonader hos försöksillrarna (Tabell 2). Kvicksilverinnehållet i vävnaderna hos såväl illrar som höns visades bestå huvudsakligen av metylkvicksilver.
Försöksresultaten ger positivt belägg för att alkylkvicksilver kan passera en näringskedja under anrikning och med till synes bibehållen toxicitet. De ekologiska konsekvenserna diskuteras.
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