More than 250 microcystins have been identified to date,[1] representing differences in the two variable residues and some modifications in the other amino acids.

In Microcystis aeruginosa microcystin-LR is synthesized by proteins that encoded by a 55 kb microcystin-gene cluster (mcy) that contains 6 large (over 3 kb) genes that encode proteins with polyketide synthase activity, nonribosomal peptide synthase activity (mcyA-E and G) and 4 smaller genes (mcyF and H-J).

[4][5] The biosynthesis of microcystin-LR in Microcystis aeruginosa begins with the coupling of phenylacetate to the mcyG enzyme.

The first steps of the synthesis involve the insertion of several carbon- and oxygen atoms between the acetyl- and phenylgroup.

This part of the synthesis is catalyzed by enzyme domains that possess β-ketoacylsynthase, acyltransferase, C-methyltransferase and ketoacyl reductase activity.

The Adda side-chain of microcystin-LR is accommodated to the hydrophobic groove, the carboxylic D-Glu site makes hydrogen bonds to metal-bound water molecules and the carboxyl group of the Masp site makes hydrogen bonds to conserved arginine and tyrosine residues in the PPP enzyme.

There are epidemiological results from studies that have shown symptoms of poisoning attributed to the presence of cyanotoxins in drinking water.

116 patients experienced multiple effects: visual disturbance, nausea, vomiting and muscle weakness.

One hundred developed acute liver failure and 52 suffered from symptoms of what is now called "Caruaru Syndrome.

[11] Acute microcystin-LR intoxication may result in long-term injury, while chronic low-level exposure may cause adverse health effects.

From animal studies, it is proven that there will be chronic liver injury from oral exposure to microcystin-LR.

Cyanobacteria prefer to live in water bodies such as lake, ponds, reservoirs, and slow-moving streams.

Together with the fact that mice with an induced higher concentration CYP450 are less affected by the toxin, this suggest that CYP450 plays an important role in the detoxification of the compound.

[19] Toxic effects cyanotoxins are very diverse and include neurotoxicity, hepatotoxicity and cytotoxicity with chemical burns.

The liver weight will increase due to intrahepatic hemorrhage, haemodynamic shock, heart failure and death.

For the assessment of possible chronic human health effects, studies involving repeated oral administration of pure microcystins at various dose levels are most desirable.

Mice treated with the carcinogenic compound dimethylbenzathracene showed an increased number and weight of skin tumors.

[10] Perhaps due to poor absorption after exposure, orally administered microscytins are less toxic, as a lethal dose in mice is about 5 to 10 μg/kg body weight.

[20] Blooms of Microcystis aeruginosa did not cause increased tumor rates in groups of mice treated for up to one year.

There is no change in the expression of selected genes involved in the cellular response to DNA damage after a 4-hour exposure.

After 24 hours, the DNA damage-responsive genes were upregulated, which indicates that microcystin-LR is an indirect genotoxic agent.

[22] In China, the highest incidence of liver cancer occurs in areas with abundant cyanobacteria in the surface waters.

[20] A metalloprotease enzyme isolated from bacteria at Lake Rotorua, among other locations, is called microcystinase.

[23] The Chinese general Zhu-Ge Liang was the first to observe cyanobacteria poisoning about 1000 years ago.

He reported the death of troops who drank green coloured water from a river in southern China.

That is the reason why the World Health Organization (WHO) issued a guideline for microcystins in drinking water.