Cyanobacterial toxins – occurrence, biosynthesis and impact on human affairs

Abstract

Mass developments of cyanobacteria ("blue-green algae") in lakes and brackish waters have repeatedly led to serious concerns due to their frequent association with toxins. Among these are the widespread hepatotoxins microcystin (MC) and nodularin (NOD). Here, we give an overview about the ecostrategies of the diverse toxin-producing species and about the genes and enzymes that are involved in the biosynthesis of the cyclic peptides. We further summarize current knowledge about toxicological mechanisms of MC and NOD, including protein phosphatase inhibition, oxidative stress and their tumor-promoting capabilities. One biotransformation pathway for MC is described. Mechanisms of cyanobacterial neurotoxins (anatoxin-a, homanatoxin-a, and anatoxin-a(s)) are briefly explained. We highlight selected cases of human fatalities related to the toxins. A special focus is given to evident cases of contamination of food supplements with cyanobacterial toxins, and to the necessary precautions.

Quantitatively evaluating detoxification of the hepatotoxic microcystins through the glutathione and cysteine pathway in the cyanobacteria-eating bighead carp

“…However, when fish was exposed to the high dosage of MC-LR, one of the most toxic microcystin variants, the balance between accumulation and detoxification was broken, i.e., the biotransformation of MC-LR to MCLR-Cys was negatively influenced, leading to substantial accumulation of MC-LR in various organs of the bighead carp. As MCLR-Cys is more water soluble than MC-LR and thus enhances the excretion of MC-LR (Dittmann and Wiegand, 2006), such a negative influence on biotransformation may also explain why MCLR-Cys content in the organs of bighead carp was lower at the high dose group in the present study.…”

“…It is well known that GSH plays a significant role in the metabolism of xenobiotics, and its conjugation with xenobiotics is considered as an important metabolic pathway for detoxification (Ketterer et al, 1983). GSH can conjugate with MC-LR via glutathione-S-transferase in various aquatic macrophyte, invertebrates, fish eggs and fish, and subsequently degraded to MCLR-Cys (Carmichael, 1992;Dittmann and Wiegand, 2006;Pflugmacher et al, 1998). In the present work, although MCLR-GSH and MCRR-GSH could be qualitatively detected occasionally in liver, kidney, intestine and muscle, their content was always below LOD, while substantial amount of MCLR/RR-Cys was detected.…”

“…Secondly, MCLR/RR-GSH might be effectively converted to MCLR/RR-Cys in kidney. Since the activity of ␥-glutamyltransferase that catalyze the conversion of MCLR-GSH to MCLR-␥-glutamylcysteine is highest in kidney (Anders, 1980;Dittmann and Wiegand, 2006), it is reasonable that MCs-Cys are effectively accumulated in kidney and that MCs-Cys are organotropic to kidney rather than to liver. In addition, after exposure to MCs, the GSH conjugation of MC-LR/RR in kidney is effectively catalyzed by increased glutathione S-transferase (GST) and subsequently degraded to MCLR/RR-Cys.…”

Massive multiplication of genome and ribosomes in dormant cells (akinetes) of Aphanizomenon ovalisporum (Cyanobacteria)

“…Major blooms have been reported in Australia, Northern Europe, India, New Zealand, South Africa, USA and the Baltic Sea (Carmichael et al, 1990;Codd et al, 1999;Hudnell et al, 2008), indicating a phenomenon of global dimensions. Many Nostocales species produce potent toxins that have been associated with livestock deaths, water quality deterioration and seafood contamination (Codd et al, 2005;Dittmann and Wiegand, 2006;van Apeldoorn et al, 2007). The ability to develop akinetes (spore-like cells) is a survival trait of the Nostocales that provides these toxic species with a competitive advantage over other phytoplankton.…”

Caracterização molecular de cianobactérias isoladas de ecossistema manguezal do Estado de São Paulo e identificação de produtos naturais

“…Dittmann et al (1997) identificaram genes envolvidos com a síntese de microcistinas em cepas de cianobactérias tóxicas confirmando a origem não ribossômica da produção de microcistinas. Esses peptídeos não ribossômicos são inibidores de proteínas fosfatases 1 e 2a (PP1/2a) e, mais frequentemente estão associados com hepatotoxicidade em mamíferos e outros vertebrados (DAWSON, 1998;WIEGAND, 2006). …”