Nephrotoxic effects of chronic administration of microcystins -LR and -YR

Milutinović, Aleksandra; Živin, Marko; Zorc-Pleskovič, Ruda; Sedmak, Bojan; Šuput, Dušan

doi:10.1016/s0041-0101(03)00143-0

Cited by 110 publications

(67 citation statements)

References 32 publications

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“…They are detrimental to water quality and negatively affect the development of nautical sports and other recreational activities (Turner et al, 1990;Giannuzzi et al, 2011). Many Microcystis strains can produce the potent hepatotoxin microcystin (MC), of which there are more than 100 variants, causing liver damage as well as nephrotoxicity (Milutinovic et al, 2003;Merel et al, 2013;Niedermeyer, 2013). Harke et al (2016) conclude that the occurrence of Microcystis toxic blooms appears to be expanding, since 108 countries or territories around the world have documented their presence in recent years compared with fewer than 30 countries in earlier years (Zurawell et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Mathematical modeling of Microcystis aeruginosa growth and [D-Leu1] microcystin-LR production in culture media at different temperatures

et al. 2017

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A B S T R A C TThe effect of temperature (26 C, 28 C, 30 C and 35 C) on the growth of native CAAT-3-2005 Microcystis aeruginosa and the production of Chlorophyll-a (Chl-a) and Microcystin-LR (MC-LR) were examined through laboratory studies. Kinetic parameters such as specific growth rate (m), lag phase duration (LPD) and maximum population density (MPD) were determined by fitting the modified Gompertz equation to the M. aeruginosa strain cell count (cells mL À1 ). A 4.8-fold increase in m values and a 10.8-fold decrease in the LPD values were found for M. aeruginosa growth when the temperature changed from 15 C to 35 C. The activation energy of the specific growth rate (Em) and of the adaptation rate (E 1 /LPD) were significantly correlated (R 2 = 0.86). The cardinal temperatures estimated by the modified Ratkowsky model were minimum temperature = 8.58 AE 2.34 C, maximum temperature = 45.04 AE 1.35 C and optimum temperature = 33.39 AE 0.55 C.Maximum MC-LR production decreased 9.5-fold when the temperature was increased from 26 C to 35 C. The maximum production values were obtained at 26 C and the maximum depletion rate of intracellular MC-LR was observed at 30-35 C. The MC-LR cell quota was higher at 26 and 28 C (83 and 80 fg cell À1 , respectively) and the MC-LR Chl-a quota was similar at all the different temperatures (0.5-1.5 fg ng À1 ).The Gompertz equation and dynamic model were found to be the most appropriate approaches to calculate M. aeruginosa growth and production of MC-LR, respectively. Given that toxin production decreased with increasing temperatures but growth increased, this study demonstrates that growth and toxin production processes are uncoupled in M. aeruginosa. These data and models may be useful to predict M. aeruginosa bloom formation in the environment.

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Section: Introductionmentioning

confidence: 99%

Mathematical modeling of Microcystis aeruginosa growth and [D-Leu1] microcystin-LR production in culture media at different temperatures

et al. 2017

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“…Some conspicuous effects of microcystin-LR were also been reported on carp kidney (Rabergh et al, 1991). Many other studies show the nephrotoxicity promoted by microcystin-LR (Kotak et al, 1996;Nobre et al, 1999;Milutinovic et al, 2002Milutinovic et al, , 2003. Human intoxications were described for populations exposed through drinking water or recreational activities (Falconer, 1999) and for many patients submitted to renal dialysis treatment (Pouria et al, 1998;Azevedo et al, 2002;Soares et al, 2006).…”

Section: Discussionmentioning

confidence: 96%

“…Several studies have reported that microcystins induce severe hepatic hemorrhage leading to shock (Runnegar and Falconer, 1982) but also can affect rat kidney, indicating microcystin to be a potential nephrotoxic (Eriksson et al, 1988(Eriksson et al, , 1989Hooser et al, 1989;Nobre et al, 1999;Milutinovic et al, 2003). Some conspicuous effects of microcystin-LR were also been reported on carp kidney (Rabergh et al, 1991).…”

Section: Discussionmentioning

confidence: 97%

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Mitochondria a key role in microcystin‐LR kidney intoxication

La-Salete

Oliveira

Palmeira

et al. 2007

J of Applied Toxicology

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Microcystins (MCs) are a group of closely related cyclic heptapeptides produced by a variety of common cyanobacteria. These toxins have been implicated in both human and livestock mortality. Microcystin-LR could affect renal physiology by altering vascular, glomerular and urinary parameters, indicating that MC-LR could act directly on the kidney. The aim of the current work was to examine the effect of MC-LR on mitochondrial oxidative phosphorylation of rat kidney isolated mitochondria.Furthermore, microcystin-LR decreased both state 3 and carbonylcyanide p-trifluoromethoxyphenylhydrazone (FCCP)-uncoupled respiration. The transmembrane potential was strongly depressed by MC-LR in a concentration dependent manner, pointing to an uncoupling effect; however, microcystin-LR did not increase the permeability of the inner mitochondria membrane to protons. Therefore, the transmembrane decrease was a consequence of a strong inhibitory effect on redox complexes. The addition of uncoupling concentrations of MC-LR to Ca 2+ + + + + -loaded mitochondria treated with ruthenium red resulted in mitochondrial permeability transition pore (MPTP) opening, as evidenced by mitochondrial swelling in isosmotic sucrose medium. Mitochondrial swelling in the presence of Ca 2+ + + + + was prevented by cyclosporin A and was drastically inhibited by catalase and dithiothreitol, indicating the participation of mitochondrial generated reactive oxygen species in this process. From this study it can be concluded that the bioenergetic lesion promoted by microcystin-LR seems to be sufficient to explain renal injury.

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“…Estudos in vitro demonstraram os efeitos citotóxicos da microcistina-LR em células humanas como eritrócitos, linfócitos, células endoteliais, epiteliais e fibroblastos (McDERMOTT et al, 1998;LANKOFF et al, 2004;SICINSKA et al, 2006), bem como em promielócitos de ratos (McDERMOTT et al, 1998) e em linfócitos de galinha e de carpas (LANKOFF et al, 2004;. Estudos in vivo relataram também efeitos nefrotóxicos em ratos (MILUTINOVIC et al, 2003), em carpas (RABERGH; BYLUND; ERIKSSON, 1991; e em trutas (KOTAK et al, 1996) e ainda, efeitos citotóxicos gastrintestinais em camundongos (BOTHA et al, 2004) e em ratos (NOBRE et al, 2004).…”

Section: Fisiopatologia Da Intoxicação Por Microcistinaunclassified

Hepatotoxicidade associada à microcistina

Santos¹,

Bracarense

2008

Sem. Ci. Agr.

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ResumoEfluentes industriais e urbanos e a intensa exploração agrícola e de pescado têm levado à eutrofização de muitos mananciais de água, destinados ao consumo e às atividades recreacionais. A eutrofização das águas, freqüentemente, tem como conseqüência o desenvolvimento expressivo de cianobactérias. Estas florações induzem a sérios problemas, visto que a ocorrência de Microcystis aeruginosa, uma das cianobactérias mais difundidas, pode produzir microcistinas (MCs). O efeito citotóxico da MC tem sido descrito no fígado, pulmões, estômago e intestino. Mortes de seres humanos, de animais silvestres e domésticos têm sido associadas à exposição a MC. Esta pode ocorrer diretamente por ingestão, inalação, contato, inoculação intravenosa (hemodiálise) ou indiretamente, pelo consumo de animais, dentre os quais os peixes e moluscos, que podem ingerir as cianobactérias e suas toxinas. A mais tóxica e também mais comum das MCs é a microcistina-LR (MC-LR), cujo órgão alvo é o fígado. A MC chega ao fígado especificamente por transporte dos ácidos biliares e, uma vez no citoplasma, inibe as proteínas fosfatases 1 e 2A, induzindo ao aumento da fosforilação protéica. Esta reação tem duas conseqüências: destruição do citoesqueleto, causando efeitos citotóxicos e descontrole da divisão celular, levando à promoção tumoral. A exposição aguda à MC induz severa hemorragia intra-hepática, necrose e apoptose, enquanto a exposição crônica pode causar neoplasia hepática ou intestinal. Também tem sido relatado que a hepatotoxicidade da MC está intimamente associada à formação intracelular de espécies reativas de oxigênio. A MC pode ser naturalmente degradada por bactérias ou pela radiação solar. Contudo, se não houver eficiente degradação, a MC poderá persistir na cadeia alimentar aquática. A contaminação de águas pela MC representa, portanto, perigo à saúde humana e de animais. Assim, esforços para evitar a eutrofização de fontes de águas são essenciais para minimizar riscos à saúde pública. Palavras-chave: Microcystis aeruginosa, microcistina, cianotoxinas, hepatotoxina AbstractUrban and industrial discharges, intense agricultural exploitation and fisheries have been causing the eutrophication in both drinking and recreational waters. A frequent consequence of eutrophication in waters is the massive development of cyanobacteria. The occurrence of these blooms induces a severe problem, as Microcystis aeruginosa, the most widespread distributed cyanobacteria, can produce microcystins (MC). Toxic effects of MC have been described in liver, lungs, stomach, and intestine. Deaths in wildlife, livestock and human beings were also associated with MC exposition. MC exposition can occurs directly by ingestion, inhalation, contact, intravenous inoculation of contaminated water (hemodialysis) or indirectly, by the consumption of animals, as fish and mollusks, the majors ingestors of cyanobacteria and its toxins. The most 1 Prof. Ass.,

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Nephrotoxic effects of chronic administration of microcystins -LR and -YR

Cited by 110 publications

References 32 publications

Mathematical modeling of Microcystis aeruginosa growth and [D-Leu1] microcystin-LR production in culture media at different temperatures

Mathematical modeling of Microcystis aeruginosa growth and [D-Leu1] microcystin-LR production in culture media at different temperatures

Mitochondria a key role in microcystin‐LR kidney intoxication

Hepatotoxicidade associada à microcistina

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