[4][5] Bongkrek acid, when consumed through contaminated foods, mainly targets the liver, brain, and kidneys along with symptoms that include vomiting, diarrhea, urinary retention, abdominal pain, and excessive sweating.

[6] During 1930s, Indonesian government went through an economic depression, and this condition caused some of the people to make tempe bongkrek by themselves, instead of buying it directly from well-trained producers.

Dutch scientists W. K. Mertens and A. G. van Veen from the Eijkman Institute of Jakarta, started to find the cause of the poisoning in the early 1930s.

B. cocovenenans is commonly found in plants and soil, which can be taken up by coconuts and corn, leading to the synthesis of bongkrek acid during the fermentation of such foods.

The way bongkrek acid works is that it interrupts the transport process of the cytosolic ADP in the inner membrane of mitochondria by inhibiting the mitochondrial ANT.

As a result, the hydrogen bonding interactions and the salt bridge put bongkrek acid in the center of the ANT active site, inhibiting the action of the translocase.

The structure of bongkrek acid-ANT shows that there are six transmembrane alpha helices covering up the active site of the ANT, preventing the binding of adenosine nucleotides.

[11][12] After consumption of bongkrek acid-contaminated corn-based or coconut-based foods, the latency period is expected to be between 1 and 10 hours.

The common symptoms of bongkrek acid poisoning are dizziness, somnolence, excessive sweating, palpitations, abdominal pain, vomiting, diarrhea, hematochezia, hematuria, and urinary retention.

The commonly used protocol to treat bongkrek acid poisoning is to remove the toxins that are not absorbed by the adenine nucleotide translocase (ANT) and to provide treatments that are specific to the symptoms that patients are having.

Due to the lack of specific treatments and antidotes for the toxins, the timing is critical to reverse the severe physiological effects.