Abstract
The effects of prolonged exposure to microcystins (MCs) on health are not yet sufficiently understood and this type of poisoning is often undiagnosed. Even though chronic exposure has been linked with liver cancer and alterations have been described in liver damage marker enzymes in exposed populations, there are not profile parameters that indicate prolonged exposure to microcystins.The aim of this work is to determine, based on an animal model of prolonged exposure to successive i.p. doses of 25 μg MC-LR/kg body weight, several plasma parameters which could be useful as exposure biomarkers.Hemoglobin (Hb) and methemoglobin (MetHb) levels were determined on blood samples. We also studied plasma levels of hydroperoxides (ROOHs), α-tocopherol, glutathione and lipid profile as well as superoxide dismutase (SOD) and catalase (CAT) erythrocyte activities. In addition, the determination of MC-LR levels in liver, kidney, plasma, urine and feces of treated mice was carried out. We found that alteration in MetHb, ROOHs, glutathione, α-tocopherol levels, SOD activity and plasma lipid profile, correlates with those expected if the alteration derived from hepatic damage. The alterated plasma paramenters together with MC-LR determination could be used as biomarkers, helpful tools in screening and epidemiological studies.
Highlights
Cyanobacterial blooms in natural waters, causing serious water pollution and public health hazard to humans and livestock, have become a worldwide problem (Carmichael, 1997; WHO, 2004)
In previous works we reported alterations in liver weights normalized to body weight, alanine transaminase (ALT) and alkaline phosphatase (ALP) activities produced by MC-LR i.p. administration
Due to the nature of the sub-chronic intoxication previously determined by our research group, we studied peripheral blood alterations related to redox status and lipid profile by assessing parameters such as ROOHs, MetHb, superoxide dismutase (SOD), CAT, glutathione, lipids, fatty acids and a-tocopherol (Andrinolo et al, 2008; Sedan et al, 2010)
Summary
Cyanobacterial blooms in natural waters, causing serious water pollution and public health hazard to humans and livestock, have become a worldwide problem (Carmichael, 1997; WHO, 2004). The two main MCs toxic mechanisms are their ability to inhibit protein phosphatases 1 and 2A (Yoshizawa et al, 1990) and enhance intracellular production of reactive oxygen species (ROS) (Ding et al, 1998), which results in significant imbalances in protein phosphorylation status and redox homeostasis (Gehringer, 2004; Ding et al, 2000, 2003). This scenario leads to hepatocyte cytoskeleton disruption (Ohta et al, 1992; Toivola et al, 1994), D. Sedan et al / Toxicon 68 (2013) 9–17 deregulation of cell division (Carmichael, 1994; Guzman et al, 2003), DNA damage (Ding et al, 1999; Lezcano et al, 2012) tumor promotion (Falconer, 1991; Falconer and Humpage, 1996), lipid peroxidation and hepatic lipid profile alterations (Andrinolo et al, 2008; Sedan et al, 2010), mitochondrial membrane permeability changes (Ding et al, 2000, 2001; Moreno et al, 2003) and apoptosis (Gehringer, 2004; Lezcano et al, 2012) according to the level, time and/or route of exposure
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