Oral toxicity of a bloom of the cyanobacteriummicrocystis aeruginosaadministered to mice over periods up to 1 year

Abstract

Cyanobacterial blooms in lakes have been reported causing livestock deaths and liver injury to human populations. In this study bloom material consisting of Microcystis aeruginosa was collected from a farm water storage after the death of sheep drinking from it. The cyanobacterial cells were lysed and a cell-free extract was provided to mice at a series of dilutions as their only source of drinking water. Mice of both sexes, with controls, were killed at intervals up to 1 yr of administration. Autopsies, histopathological examination, and analyses of plasma lactate dehydrogenase and alanine aminotransferase were carried out. Increased mortality was observed, particularly among males, together with chronic active liver injury and elevated alanine aminotransferase in blood. In control mice and those receiving lower concentrations of extract, hepatic amyloidosis with neutrophil infiltration, and bronchopneumonia, were seen with increasing age. The bronchopneumonia appeared earlier among mice receiving cyanobacterial extract. Four tumors were seen in 71 mice receiving a high concentration of extract for up to 1 yr, none in 150 mice receiving lower concentrations, and 2 in 73 control mice. No effects on male or female fertility, embryonic mortality, neonatal viability, or skeletal development were observed, but 7 out of 73 neonatal mice born to parents given cyanobacterial extract showed reduced brain size. No cases were seen in controls. We conclude that the major toxicity exhibited is liver injury. Further attention is needed for evaluation of carcinogenicity and embryonic damage.

A proteomic analysis of prenatal transfer of microcystin-LR induced neurotoxicity in rat offspring

“…PCNA can associate with several procaspases to block their activation for presenting anti-apoptotic activities [73,74]. These reports and the present results altogether suggest that MCs may induce apoptosis and inflammatory in the brain [12,13].…”

“…More recently, several OATPs/Oatps (rodent Oatp) appear to be specifically required for the active uptake of MCs into brain [10][11][12]. In fish, Baganz et al reported changes in the spontaneous locomotor behavior of zebrafish (Danio rerio) and sunbleak (Leucaspius delineatus) after MCLR exposure [13,14] and Cazenave et al showed changes in swimming activity of Jenynsia multidentata fed with microcystin-RR (MCRR) [15], suggesting the probable neurotoxicity of MCs. In mammals, spatial learning and memory loss were observed in rats after intra-hippocampal infusion with MCLR [15,17].…”

Cyanobacterial toxins: removal during drinking water treatment, and human risk assessment.

“…The liver is the major target organ for microcystin toxicity; it was shown to accumulate 20-70% of a radioactively labeled toxin dose (intravenous) (48)(49)(50)(51)(52)(53)(54). Studies in mice and pigs exposed to extracts of a toxic M. aeruginosa bloom demonstrated dosedependent toxicity (55,56). Increased mortality, liver weight, and plasma alanine aminotransferase levels were associated with loss of body weight.…”

Developmental Biology of Neoplastic Growth

“…The waterblooms of toxic cyanobacteria (blue-green algae), found in eutrophic freshwater municipal and residential water supplies, are an increasing environmental hazard in several areas of the world (Francis 1878;Carmichael 1988;Falconer et al 1998). Microcystins are cyclic heptapeptides containing two variable l-amino acids and an unusual amino acid, 3-amino-9-methoxy-10-phenyl-2,6,8-trimethyl-deca-4,6-dienoic acid (Adda) (Fig.…”