About 125 people who had been swimming in the sea get suffered from symptoms like itching, burning, blisters, rash and desquamation.

Samples of L. majuscula revealed that this blue-green alga contained a mixture of aplysiatoxin, debromoaplysiatoxin and lyngbyatoxin A.

After taking samples of this red alga it turned out that they contained two toxins which were identical with aplysiatoxin and debromoaplysiatoxin.

In view of the fact that some blue-green alga like L. majuscula produce aplysiatoxin and debromoaplysiatoxin, it's probable that they are the true origin of this food poisoning case.

This compound combines spiro acetal, hemiacetal and diolide functionalities, which result in peculiar biological activities.

[4] To this date, only Yoshita Kishi's approach to synthesize debromoaplysiatoxin from scratch was found to be effective.

This intermediate can be converted into a terminal epoxide by usage of classical synthetical operations, such as introducing acetic acid or substitution reactions with tosylates.

Therefore, the β-keto thioester is formed out of the alcohol by a quadruplet of reactions with respectively N,N′-dicyclohexylcarbodiimide (DCC), N-chlorosuccinimide (NCS), sodium chlorite and 1,1'-carbonyldiimidazole (CDI).

With 2,3-dichloro-5,6-dicyano-1,4-benzoquinone (DDQ) treatment, this β-keto thioester can be converted into an unstable diol, which is the acyclic precursor of the end product.

Because the analogues possess the skeleton of tumor-promoting aplysiatoxin and debromoaplysiatoxin, the adverse effects would be most likely tumor promotion.

Examination of the structure–activity relationship (SAR) of this hydrophobic region showed that the absence of the brominated molecule in moieties of Lyngbya toxins reduced malignant transformation and DNA synthesis in cells.

Lethargy (a state of tiredness, weariness, fatigue, or lack of energy), muscular contractions and sometimes hind leg paralysis were observed.

It may be hypothesized that the continual presence of these toxin-producing cyanobacteria on the skin of these clinically ill animals may be contributing to their dermatologic disease.

[10] (5) In rabbits and hairless mice topical application of debromoaplysiatoxin produced severe cutaneous inflammatory reactions.

This inflammation response and the mechanism of tumor promotion is likely to be mediated through activation of calcium activated, phospholipid-dependent protein kinase C.[11] In the aplysiatoxin class, debromoaplysiatoxin, aplysiatoxin, and 19-bromoaplysiatoxin have been found to be tumor promoters in mouse skin.

Also rat tracheal cells in culture are sensitive indicators for the presence of the polyacetates, aplysiatoxin and debromoaplysiatoxin.

It causes increase in colony formation and is in agreement with a proliferative activation ('triggering') of the basal cell population from the normally quiescent Go state found in intact tracheal epithelium.