Publications by authors named "Priscila A Rossi"

Microcystins (MC) are hepatotoxic for organisms. Liver MC accumulation and structural change are intensely studied, but the functional hepatic enzymes and energy metabolism have received little attention. This study investigated the liver and hepatocyte structures and the activity of key hepatic functional enzymes with emphasis on energetic metabolism changes after subchronic fish exposure to cyanobacterial crude extract (CE) containing MC.

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The effects of cypermethrin-based insecticide (CBI), commonly used in aquaculture and agriculture, were evaluated in matrinxa (Brycon amazonicus) exposed to sub-lethal concentration (20% of LC50) for 96 h. Physiological and biochemical effects were studied through biomarkers: lipid peroxidation (LPO), glutathione (GSH), and ascorbic acid concentrations; superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glucose-6-phosphate dehydrogenase (G6PDH) assays in the liver and gills. Besides, ions Na, Cl, and K; protein and glucose concentrations were measured in the plasma.

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The toxicological effect of cellular extract of cyanobacterium Radiocystis fernandoi strain R28 containing RR and YR microcystins was analyzed in the fish Hoplias malabaricus with emphasis on the liver structure and energetic metabolism, after short-term exposure. Fish were intraperitoneally (i.p.

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Metabolic adjustments were studied in channel catfish Ictalurus punctatus exposed to 1.5 mg L-1 of phe nol (10% LC50) for four days and recovered for seven days. Lower triacylglycerol (TGA) stores and increased muscle fat free acids (FFA) suggest fat catabolism in muscle.

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Fish parasites are among the crucial limiting factors in aquaculture. The organophosphorous pesticide trichlorfon is widely used as an insecticide and against fish parasites worldwide. In this study, the effects of environmental trichlorfon on biochemical and physiological parameters were investigated in Piaractus mesopotamicus (pacu), a widely farmed fish in South America, through sublethal exposure (8 µg L(-1), 10 % of the LC50; 96 h) and recovery.

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