Abstract
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. Remarkable liver FFA decrease (-31%) suggests liver fat catabolism as well. Increased muscular ammonia levels and ASAT (aspartate aminotransferase) and decreased plasma aminoacids suggest higher muscular amino acid uptake. Constant levels of glucose and increased liver glycogen stores, associated with lower amino acids in plasma, indicate gluconeogenesis from amino acids. This is supported by higher hepatic ALAT and ASAT. Higher hepatic LDH followed by lower plasma lactate may indicate that plasma lactate was also used as gluconeogenic substrate. Biochemical alterations were exacerbated during the post-exposure recovery period. Reduction in muscle and plasma protein content indicate proteolysis. A higher rate of liver fat catabolism was resulted from a remarkable decrease in hepatic TGA (-58%). Catabolic preference for lipids was observed in order to supply such elevated energy demand. This study is the first insight about the metabolic profile of I. punctatus to cope with phenol plus its ability to recover, bringing attention to the biological consequences of environmental contamination.
Highlights
Phenols and their derivatives are aromatic, organic compounds present in a wide variety of biotic and abiotic factors, and under numerous circumstances, they can be considered pollutants
The energy demanded to cope with poisoning was clearly observed in white muscle of I. punctatus
Increase in the glycolytic activity in white muscle of I. punctatus could be inferred by the presence of less glucose
Summary
Phenols and their derivatives are aromatic, organic compounds present in a wide variety of biotic and abiotic factors, and under numerous circumstances, they can be considered pollutants. Domestic and industrial effluents are the major source of such pollutants in aquatic environments, causing damages at several levels of biological organization (Moens et al 2007). Despite the maximum limit for the concentration of phenol in treated effluents (0.5 mg L-1) and freshwater (0.003 - 1 mg L-1) be restrictive in Brazil (Brasil 2005, Cetesb 2014a), phenol contamination in water basins is often from either industrial wastewaters or accidental phenol discharges. Total phenols concentrations are above the allowed limit in some Brazilian freshwater and coastal water points (Cetesb 2014b). It spreads out to body compartments and causes several physiological disturbances as hematological and metabolic disorders (Hori et al 2006, Avilez et al 2008, Moraes et al 2015). Multiple mechanism of action of phenol or some phenolic compounds have been reported, including: drug antagonists (Roche and Bogé 2000), induction of genotoxicity (Bolognesi et al 2006), carcinogenesis and mutagenesis (Tsutsui et al 1997, Yin et al 2006), endocrine disruption (Kumar and Mukherjee 1988), and metabolic disruption (Hori et al 2006)
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