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1.
J Exp Zool ; 218(3): 321-6, 1981 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-7040596

RESUMO

Salmo gairdneri specimens were exposed for 4-48 hours to three different concentrations of un-ionized ammonia (UIA). An increase in lysosomal sensitivity to osmotic shock and in total proteolytic activity occurs in the liver. The amount of this increase depends upon the exposure time or upon environmental and tissue ammonia levels. On the other hand ammonia does not affect lysosome hydrolases activity in vitro.


Assuntos
Amônia/farmacologia , Fígado/efeitos dos fármacos , Cloreto de Amônio/farmacologia , Animais , Endopeptidases/metabolismo , Peixes , Fígado/enzimologia , Fígado/fisiologia , Lisossomos/efeitos dos fármacos , Lisossomos/enzimologia , Lisossomos/fisiologia
2.
Artigo em Inglês | MEDLINE | ID: mdl-6128170

RESUMO

1. In Salmo gairdneri specimens exposed to 450 micrograms/l NO2-N (nearly 36 hr LC50) for various exposure times (12-72 hr) some parameters of liver lysosomal function were examined. 2. In vivo both total proteolytic activity and single protease activities were inhibited, the inhibition increasing with the lengthening of exposure time. In vitro no analogous effect was observed. 3. Lysosomal membranes showed an increased fragility correlated with the physiological conditions of treated animals. 4. Data were considered as the results of a nitrite mediated effect on functional and structural proteins.


Assuntos
Lisossomos/efeitos dos fármacos , Nitritos/intoxicação , Salmonidae/metabolismo , Truta/metabolismo , Animais , Catepsina B , Catepsinas/metabolismo , Concentração de Íons de Hidrogênio , Leucil Aminopeptidase/metabolismo , Fígado/enzimologia , Lisossomos/enzimologia , Peptídeo Hidrolases/metabolismo , Fatores de Tempo
3.
Ecotoxicol Environ Saf ; 8(2): 106-17, 1984 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-6425036

RESUMO

Salmo gairdneri specimens were exposed for 4 months to 1-10 micrograms/liter of Cd and 30-100 micrograms/liter of Cu. At different times from the beginning of the experiment the activity of some metal-sensitive enzymes was assayed (blood catalase and carbonic anhydrase; liver aminolevulinate dehydrase and total leucylaminopeptidase ). Biochemical indices of mitochondrial (respiratory control ratio; O2 consumption) and lysosomal function (percentage free leucylaminopeptidase activity), gill sialic acid content, and mucus lysozyme concentration were also detected. Cu (at both the levels tested) and Cd (only at the highest concentration) cause a remarkable alteration in various biochemical/physiological parameters under study. Considerations about the water quality criteria levels proposed by EIFAC /FAO for the two metals are reported.


Assuntos
Cádmio/toxicidade , Cobre/toxicidade , Salmonidae/metabolismo , Truta/metabolismo , Abastecimento de Água/normas , Animais , Anidrases Carbônicas/sangue , Catalase/sangue , Brânquias/enzimologia , Leucil Aminopeptidase/metabolismo , Fígado/enzimologia , Lisossomos/enzimologia , Mitocôndrias Hepáticas/metabolismo , Muramidase/metabolismo , Consumo de Oxigênio/efeitos dos fármacos , Sintase do Porfobilinogênio/sangue , Ácidos Siálicos/metabolismo , Pele/enzimologia , Poluentes Químicos da Água/toxicidade
4.
Environ Res ; 34(1): 135-54, 1984 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-6723603

RESUMO

In Salmo gairdneri specimens exposed for 12, 24, 48, and 72 hr to nitrite (450 micrograms NO2-N) the main biochemical parameters of cerebral and hepatic hypoxia were studied. Observations on liver ultrastructure were also made to follow nitrite hepatotoxicity. Furthermore, some physiological alterations in liver mitochondria incubated in a medium containing a nitrite concentration similar to that found in the liver of in vivo exposed trout were studied. Results suggest that tissue hypoxia, due to the nitrite-induced high methemoglobinemia, is too low to be directly responsible for animal death. Nevertheless liver hypoxia is thought to be at the root of nitrite acute toxicity mechanism by producing suitable conditions for toxic potentialities. Thus irreversible and deadly damages arise in liver biochemistry and ultrastructure, particularly at the mitochondrial level.


Assuntos
Fígado/efeitos dos fármacos , Nitritos/toxicidade , Oxigênio , Trifosfato de Adenosina/análise , Animais , Química Encefálica/efeitos dos fármacos , Lactatos/análise , Ácido Láctico , Fígado/análise , Fígado/ultraestrutura , Metemoglobina/análise , Mitocôndrias Hepáticas/efeitos dos fármacos , Truta
5.
Ecotoxicol Environ Saf ; 6(5): 479-88, 1982 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-7169039

RESUMO

Goldfish specimens were exposed for 24-48 hr to 20, 40, 600, and 2500 micrograms N/liter unionized ammonia (UIA). This treatment causes, in the brain, increases in total ammonia, glutamine, lactate, and succinate and decreases in glutamate, glucidic stores, total NADH, and ATP. Most of these effects have already been reported in ammonia-treated trout. It is therefore suggested that the cerebral biochemical mechanisms of ammonia toxicity in these two species are fundamentally the same. The most important metabolic alterations, however, appear for UIA concentrations which are higher than those necessary to produce the same effects in trout, in accordance with the greater resistance of goldfish to ammonia. Some of the physiological-biochemical adaptations which are at the root of this phenomenon have been pointed out and discussed. In the liver of the ammonia-treated goldfish total ammonia, glutamine, glutamate, and succinate all increase, while lactate, glycine, and taurine decrease; liver glucidic stores remain unaltered. These results indicate a difference in the metabolic responses of goldfish and trout liver.


Assuntos
Adaptação Fisiológica , Amônia/toxicidade , Cyprinidae/metabolismo , Carpa Dourada/metabolismo , Poluentes Químicos da Água/toxicidade , Poluentes da Água/toxicidade , Amônia/metabolismo , Animais , Encéfalo/metabolismo , Glutamina/metabolismo , Fígado/metabolismo , Succinatos/metabolismo , Truta/metabolismo
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