Pathological and Biochemical Characterization of Microcystin-Induced Hepatopancreas and Kidney Damage in Carp (Cyprinus carpio)

Abstract

The presence of apoptotic cell death was determined using in situ fragment end labeling (ISEL) of the respective tissue sections and agarose gel electrophoresis for detection of DNA-laddering. The analysis of carp tissue extracts (hepatopancreas, kidney, GI tract, skeletal muscle, brain, heart, spleen, and gills) demonstrated MC-LR adducts having molecular weights of 38 kDa (putatively catalytic subunit of protein phosphatases-1 and -2A) and 28 kDa, respectively. An additional band was found to be present at 23 kDa in both hepatopancreas and kidney. The present data demonstrate that, in comparison to the pathological events in salmonids exposed to MC, where a slower development of pathology and primarily necrotic cell death prevails, the pathology in carp develops rapidly and at lower toxin concentrations. This is most likely due to a more efficient uptake of toxin, while the mechanism of cell death is primarily apoptosis.

Plasma biochemical responses of the omnivorous crucian carp (Carassius auratus) to crude cyanobacterial extracts

“…Marked blood biochemical responses often occur after aquatic organisms have been exposed to microcystins, with injury of organs (Råbergh et al 1991;Fischer and Dietrich 2000;Malbrouck et al 2003Malbrouck et al , 2006Zhang et al 2007). MC-induced liver damage has been correlated with the elevation of the activity of some plasma enzymes, for example alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) (Fischer and Dietrich 2000;Malbrouck et al 2003Malbrouck et al , 2006Molina et al 2005).…”

“…MC-induced liver damage has been correlated with the elevation of the activity of some plasma enzymes, for example alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) (Fischer and Dietrich 2000;Malbrouck et al 2003Malbrouck et al , 2006Molina et al 2005). Pathological alterations in the blood activities of these enzymes are generally a result of hepatocyte leakage after cellular alteration or damage (Bernet et al 2001;Malbrouck et al 2006).…”

Global effects of subchronic treatment of microcystin-LR on rat splenetic protein levels

“…Studies demonstrated that MC accumulation could lead to the production of reactive oxygen species (ROS) [5,6], followed by destruction of the cytoskeleton, leading to cell necrosis, apoptosis and hemorrhage [7,8].…”

“…MCs accumulated mainly in liver and were known for their hepatotoxic effects [7,9]. However, MCs could also accumulate in other organs such as the kidney [10,11] and the brain [12], eventually resulting in damage to these organs.…”

Mitochondria a key role in microcystin‐LR kidney intoxication

“…Furthermore, they release mediators capable of promoting nephotoxicity in isolated perfused rat kidney (Nobre et al, 1999), involving phospholipase A 2 and a cyclooxygenase in this process (Nobre et al, 2003). Many authors have already shown that MC-LR promotes renal alterations and affects renal physiology (Wickstrom et al, 1995;Nobre et al, 1998;Beasley et al, 2000;Fischer and Dietrich, 2000;Milutinovic et al, 2002). Since renal mitochondrial bioenergetics plays a crucial role in cellular metabolism, the main objective of this work was to evaluate the effects of microcystin-LR on isolated kidney mitochondria.…”