SUMMARYEarlier studies demonstrated that oscars, endemic to ion-poor Amazonian waters, are extremely hypoxia tolerant, and exhibit a marked reduction in active unidirectional Na + uptake rate (measured directly) but unchanged net Na + balance during acute exposure to low P O2 , indicating a comparable reduction in whole body Na + efflux rate. However, branchial O 2 transfer factor does not fall. The present study focused on the nature of the efflux reduction in the face of maintained gill O 2 permeability. Direct measurements of 22 Na appearance in the water from bladder-catheterized fish confirmed a rapid 55% fall in unidirectional Na + efflux rate across the gills upon acute exposure to hypoxia (P O2 =10-20 torr; 1 torr=133.3 Pa), which was quickly reversed upon return to normoxia. An exchange diffusion mechanism for Na + is not present, so the reduction in efflux was not directly linked to the reduction in Na + influx. A quickly developing bradycardia occurred during hypoxia. Transepithelial potential, which was sensitive to water [Ca 2+ ], became markedly less negative during hypoxia and was restored upon return to normoxia. Ammonia excretion, net K + loss rates, and 3 H 2 O exchange rates (diffusive water efflux rates) across the gills fell by 55-75% during hypoxia, with recovery during normoxia. Osmotic permeability to water also declined, but the fall (30%) was less than that in diffusive water permeability (70%). In total, these observations indicate a reduction in gill transcellular permeability during hypoxia, a conclusion supported by unchanged branchial efflux rates of the paracellular marker [ 3 H]PEG-4000 during hypoxia and normoxic recovery. At the kidney, glomerular filtration rate, urine flow rate, and tubular Na + reabsorption rate fell in parallel by 70% during hypoxia, facilitating additional reductions in costs and in urinary Na + , K + and ammonia excretion rates. Scanning electron microscopy of the gill epithelium revealed no remodelling at a macro-level, but pronounced changes in surface morphology. Under normoxia, mitochondria-rich cells were exposed only through small apical crypts, and these decreased in number by 47% and in individual area by 65% during 3 h hypoxia. We suggest that a rapid closure of transcellular channels, perhaps effected by pavement cell coverage of the crypts, allows conservation of ions and reduction of ionoregulatory costs without compromise of O 2 exchange capacity during acute hypoxia, a response very different from the traditional osmorespiratory compromise.

The Vicuña oil tanker exploded in Paranaguá Bay (South of Brazil), during methanol unloading operations in front of Paranaguá Harbour, on November 15th, 2004, releasing a large amount of bunker oil and methanol. Two weeks after the accident, the acute effects of the Vicuña Oil Spill (VOS) were evaluated in the demersal catfish Cathorops spixii, comparing a contaminated (at the spill site) and a reference site inside the Bay. Data were compared to previous measurements, taken before the accident, in the same species, from the same sites. The physiological biomarkers were the ones that best reflected acute effects of the spill: plasma osmolality, chloride, calcium, magnesium, and potassium. Morphological (liver and gill histopathology) and genetic (piscine micronucleus and DNA strand breaks) biomarkers revealed that damage was already present in fishes from both reference and contaminated sites inside the Bay. Thus, the reference site is not devoid of contamination, as water circulation tends to spread the contaminants released into other areas of the Bay. Acute field surveys of oil spill effects in harbour areas with a long history of contamination should thus be viewed with caution, and whenever possible previous evaluations should be considered for proper appraisal of biomarker sensitivity, especially in mobile bioindicators such as fish.

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Coastal and estuarine areas can be impacted by several sources of anthropogenic activities derived from industries, agriculture, sewage and harbor activities. Two Brazilian estuarine areas (Piraquê-ES e Paranaguá-PR) located close to harbours, industries and sewage from urban centers were evaluated through analysis of somatic indexes, histopathological, biochemical and genetic biomarkers on fish. Histopathological lesions as lamellar fusion, hyperplasia, epithelial lifting, and second lamellae disorganization were found in gills. Necrosis was the main alteration observed in the liver of sampled animals and the occurrence of melano-macrophages in Cathorops spixii was similar among the evaluated areas. Cholinesterase activity increased in most of the contaminated areas. Genotoxic responses as micronucleus induction and occurrence of DNA strand breaks were detected in Piraquê and Paranaguá estuaries in all sampling seasons. Our results suggest that these areas are impacted by anthropogenic activities and that a multi-biomarker approach is valuable and recommended for environmental pollution evaluation.

Light polycyclic aromatic hydrocarbons (PAHs) of petrogenic origin are commonly found in estuaries and coastal areas. Though they are known to be toxic to fish, little is known about their uptake and tissue distribution. This paper reports on the results of a study on uptake, elimination, and tissue distribution of three waterborne 14C-labeled PAHs in the mummichog, Fundulus heteroclitus, using whole-body autoradiography. After a 24 h exposure to 1 μCi·L(-1) of 14C-naphthalene, 14C-1-naphthol, and 14C-phenanthrene, fish were transferred to clean water and tissue distribution examined after 0, 1, 3, 7, 14, and 21 days of depuration. All compounds were readily accumulated by fish and were also rapidly eliminated (t0.5 range=1.1 to 3.0 days). Most of the radioactivity in naphthalene- and phenanthrene-treated fish was found in gall bladder≫liver>intestinal lumen. In naphthol-exposed fish, an important labeling of some brain areas was observed. Brain of naphthalene-exposed fish was also labeled after 24 h depuration, indicating that exposure to naphthalene may result in metabolite accumulation in the brain. This is the first study showing that naphthalene, naphthol, and/or unidentified metabolite(s) can accumulate in brain tissues, which may impair normal brain function.