Carbamazepine (CBZ) induced enzymatic stress in gill, liver and muscle of a common carp, Cyprinus carpio

Chronic toxicity of the antiepileptic carbamazepine on the clam Ruditapes philippinarum

“…This drug has antiepileptic and psychotropic properties, exerting its effects by blocking the sodium channels of excitatory neurons (Malarvizhi et al, 2012). The high consumption and the low degradation rate upon WWTPs (b 10%) (Zhang et al, 2008) are the principal reasons for the occurrence of CBZ in water bodies, namely in WWTP influents and effluents, surface waters, groundwater and even in treated drinking water, with concentrations ranging from 0.03 to 6.3 μg/L (Ternes, 1998;Sacher et al, 2001;Ferrari et al, 2003;Metcalfe et al, 2003;Bahlmann et al, 2009Bahlmann et al, , 2012Calisto et al, 2011a).…”

“…Furthermore, since CBZ is a persistent drug when released into the environment, requiring between 4.5 and 25 sunny summer days for its elimination (Calisto et al, 2011b), the evaluation of a long-term exposure is necessary to fully understand the impact of persistent drugs on aquatic organisms. Studies focusing on acute toxicity found that, in general, the CBZ concentrations causing effects occur in the mg/L range (Malarvizhi et al, 2012), which are not representative of those concentrations occurring in the aquatic ecosystem, thus, leading to conclude that the risk of acute toxic effects in the environment is unlikely (Fent et al, 2006). However, considering that pharmaceutical drugs are continuously discharged into aquatic media, the assessment of chronic toxicity is of upmost importance.…”

Morphological alterations and acetylcholinesterase and monoamine oxidase inhibition in liver of zebrafish exposed to Aphanizomenon flos-aquae DC-1 aphantoxins

“…The entry/accumulation of toxins in the liver may increase protein and carbohydrate metabolism to account for the energy crisis or need for detoxification during stress, leading to increased ALT and AST activities (De Smet and Blust, 2001;Malarvizhi et al, 2012). The results of the current and previous studies thus suggest that ALT and AST activities in zebrafish liver may be induced by aphantoxins/PSPs in response to the increased metabolism associated with hepatic dysfunction and liver structural damage (Loteste et al, 2013).…”

“…Increases in ALT and AST in zebrafish liver may represent a metabolic compensation mechanism to react with environmental toxicants by altering and adapting their metabolic functions (Malarvizhi et al, 2012). The entry/accumulation of toxins in the liver may increase protein and carbohydrate metabolism to account for the energy crisis or need for detoxification during stress, leading to increased ALT and AST activities (De Smet and Blust, 2001;Malarvizhi et al, 2012).…”

Respiratory toxicity of cyanobacterial aphantoxins from Aphanizomenon flos-aquae DC-1 in the zebrafish gill

“…The activities of AST and ALT were investigated in the gills of aphantoxin-exposed zebrafish because these enzymes are valuable biomarkers for cellular impairment, branchial dysfunction, and gill structural damage (Malarvizhi et al, 2012). Several previous studies have reported that branchial AST and ALT enzyme activities were increased as a result of exposure to heavy metals and chemicals in fish (Malarvizhi et al, 2012;Mary et al, 2014).…”