cyanoginosin-lr and Abnormalities--Drug-Induced

Apart from infections and habitat loss, environmental pollution is another major factor of global decline of amphibians. Using the model of Xenopus laevis embryos, we test the hypothesis that combined exposure of amphibians to natural toxins and anthropogenic pollutants induces more pronounced adverse effects than single exposures.. Experimental procedures adhered to Frog Embryo Teratogenesis Assay - Xenopus standards (FETAX). Exposure groups included controls, solvent (dimethyl sulfoxide) controls, and embryos exposed for 96 h to single, double and triple action of paraoxon (P), bromadiolone (B), and microcystin-LR (M), added to the FETAX medium at a dose of 300, 350, and 500 μg.L(-1), respectively. Studied responses of X. laevis embryos included mortality and malformations, head-to-tail length, total antioxidant capacity, lipid peroxidation, and caspase-3 activity.. The triple combination induced the highest mortality. Malformations in embryos significantly prevailed only in B-, and B+P-exposure groups. Apart from the single exposure to B, the tested substances and their combinations inhibited the embryonic growth. Triple exposure had the most pronounced effect both on the growth inhibition and total antioxidant capacity. Lipid peroxidation was increased after B+M exposure, while single and combined exposures to B and P had an opposite effect.. This study helps to understand adverse effects of environmental pollution by natural toxins and agrochemicals in amphibians. The results allow for risk assessment of environmental pollution and findings of low concentrations of contaminants in aquatic environments. Further research to address issues such as mixture toxicity to metamorphosing and adult amphibians is necessary.

Topics: 4-Hydroxycoumarins; Abnormalities, Drug-Induced; Animals; Anticoagulants; Body Size; Caspase 3; Cholinesterase Inhibitors; Embryo, Nonmammalian; Enzyme Inhibitors; Lipid Peroxidation; Marine Toxins; Microcystins; Paraoxon; Toxicity Tests; Xenopus laevis

The zooplankton grazer Daphnia magna endures living in water bodies up to moderate densities of cyanobacteria, such as Microcystis spp., known for producing toxic secondary metabolites. Although daphnids are affected via decreased food filtering, inhibition of digestive proteases and lethality, development of tolerance against cyanobacterial toxins has also been observed. Aim of our study was to investigate in detail chronic effects of cyanobacterial toxins, with emphasis on microcystin, on D. magna. The animals were exposed chronically for two generations to either microcystin-LR in 5 or 50 microg L(-1), or to cyanobacterial crude extract containing the same amount of total microcystin, starting at neonate stadium. Survival, growth, maturation and fecundity were observed for the first generation during two months. In the offspring survival, maturation, and growth were followed for the first week. Low concentration of microcystin-LR slightly affected the growth and reproduction of parent daphnids. Survivorship decreased during chronic exposure with increasing microcystin concentration. Age to maturity of the offspring increased and their survival decreased after parent generation was exposed to the toxin, even if the offspring were raised in control medium. Besides, cessation of the eggs/embryos was observed and malformation of neonates caused by cyanobacterial toxins was firstly recorded.

Topics: Abnormalities, Drug-Induced; Animals; Animals, Newborn; Cyanobacteria; Daphnia; Female; Growth; Larva; Marine Toxins; Microcystins; Microcystis; Reproduction; Scenedesmus; Survival

Blooms of cyanobacteria or blue-green algae are known to have caused poisoning in fish, waterfowl, animals and man. One of the toxins responsible for this is the hepatotoxin microcystin-LR which has been found to occur in blooms present intermittently in sources used for domestic water supplies. Three sets of experiments were undertaken to investigate the acute toxicity of microcystin-LR in mice and rats by the oral and intraperitoneal routes, the potential for effects on foetal development in the mouse, and the effects of repeated oral dosing over 13 weeks in the mouse. The results of this work were as follows: (1) Microcystin-LR is 30-100 times less toxic via oral ingestion than via intraperitoneal injection; (2) Microcystin-LR is not a selective developmental toxicant in the mouse. There was a No Observed Adverse Effect Level (NOAEL) of 600 microg kg(-1) bodyweight per day given on days 6-15 of pregnancy for any form of developmental toxicity; (3) There was a clear NOAEL for tissue damage in the liver of 40 microg kg(-1) bodyweight per day of microcystin-LR. Using this data, a value of 1 microg l(-1) microcystin-LR would be an appropriate guideline value for drinking water.

Topics: Abnormalities, Drug-Induced; Administration, Oral; Animals; Bacterial Toxins; Embryonic and Fetal Development; Female; Injections, Intraperitoneal; Lethal Dose 50; Liver; Male; Marine Toxins; Mice; Microcystins; No-Observed-Adverse-Effect Level; Osteogenesis; Peptides, Cyclic; Pregnancy; Rats; Toxicity Tests