The effect of the myotoxic Lys49 phospholipase A(2) from Agkistrodon contortrix laticinctus snake venom on Na+/K+ -ATPase activity of toad bladders.

ACLMT is a myotoxic Lys49 phospholipase A(2) isolated from the venom of the snake Agkistrodon contortrix laticinctus. We have previously shown that ACLMT increases baseline water transport and partially inhibits vasopressin-stimulated water transport across toad bladders due to an increase in cytosolic calcium. However, these evidences provide insufficient insight into the mechanisms involved in the effects of ACLMT on membrane permeability. In an attempt to better understand such mechanisms, the current study aimed to investigate whether the Na(+)/K(+)-ATPase activity of isolated toad bladders can be affected by the ACLMT and the synthetic peptide from its C-terminal region. The toxin significantly decreased the Na(+)/K(+)-ATPase, while the peptide did not alter it. These findings suggest that the effects of ACLMT on membrane permeability may be due to the inhibition of the Na(+)/K(+)-ATPase activity, and that the C-terminal region may not play a relevant role in this effect. This study contributes toward a better understanding of the mechanisms involved in the toxicity of the snake venom Lys49 PLA(2) myotoxins on biological tissues.

Hematological and physiological changes induced by short-term exposure to copper in the freshwater fish, Prochilodus scrofa

Hematological and physiological changes in the blood of juveniles of the freshwater fish, Prochilodus scrofa were determined after acute exposure to 20, 25, and 29 mugCu L-1 in water (pH 7.5; hardness 24.5 mg L-1 as CaCO3) for 96 h. Copper exposure to 25 and 29 mugCu L-1 caused significant increase in the hematocrit and red blood cell values. The increase in red blood cells was associated with increase in whole blood hemoglobin only in fish exposed to 29 mugCu L-1. Leukocytes increased following copper exposure and were significantly higher in fish exposed to 29 mugCu L-1. Differential leukocyte percentage displayed significant reduction in lymphocytes and an increase in neutrophils in fish exposed to 25 and 29 mugCu L-1. The percentage of monocytes remained unchanged after copper exposure. The thrombocytes did not change. There was a significant decrease in plasma [Na+] and [Cl-] and a significant drop in blood pH in fish exposed to 25 and 29 mugCu L-1 while [K+] showed significant increase in fish exposed to 29 mugCu L-1. Copper exposure led to ionoregulatory impairment, although chloride cell hypertrophy was induced. The changes in red blood cells suggest a compensatory response to respiratory surface reduction of gills (tissue damage and cell proliferation) in order to maintain oxygen transference from water to the tissues, allowing the fish to survive during the so-called shock phase of LC50 exposure, at least while at rest

Hematological and physiological changes induced by short-term exposure to copper in the freshwater fish, Prochilodus scrofa.

Hematological and physiological changes in the blood of juveniles of the freshwater fish, Prochilodus scrofa were determined after acute exposure to 20, 25, and 29 microgramsCu L-1 in water (pH 7.5; hardness 24.5 mg L-1 as CaCO3) for 96 h. Copper exposure to 25 and 29 microgramsCu L-1 caused significant increase in the hematocrit and red blood cell values. The increase in red blood cells was associated with increase in whole blood hemoglobin only in fish exposed to 29 microgramsCu L-1. Leukocytes increased following copper exposure and were significantly higher in fish exposed to 29 microgramsCu L-1. Differential leukocyte percentage displayed significant reduction in lymphocytes and an increase in neutrophils in fish exposed to 25 and 29 microgramsCu L-1. The percentage of monocytes remained unchanged after copper exposure. The thrombocytes did not change. There was a significant decrease in plasma [Na+] and [Cl-] and a significant drop in blood pH in fish exposed to 25 and 29 microgramsCu L-1 while [K+] showed significant increase in fish exposed to 29 microgramsCu L-1. Copper exposure led to ionoregulatory impairment, although chloride cell hypertrophy was induced. The changes in red blood cells suggest a compensatory response to respiratory surface reduction of gills (tissue damage and cell proliferation) in order to maintain oxygen transference from water to the tissues, allowing the fish to survive during the so-called shock phase of LC50 exposure, at least while at rest.