Ocular Hypotonia and Transient Decrease of Vision as a Consequence of Exposure to a Common Toad Poison

The common toad produces venom (bufotoxin) that is produced in the parotid gland of the toad as well as in the skin. This toxic compound is a potent inhibitor of Na+/K+-ATPase activity. Physiological effects of bufotoxin are similar to those of digitalis and cause increased heart rate and muscle contractions. Ocular toxicity was described. A 67-year-old female patient was admitted to the emergency service because of sudden vision loss and a burning sensation in both eyes after she had been exposed to the poison of a toad. Slit lamp examination showed conjunctival hyperaemia and signs of ocular hypotonia. Topical antibiotic treatment was administered, and after 24 hours, corneal oedema and ocular hypotonia were in remission. Inhibition of Na+/K+-ATPase is a well-known effect of the toad venom. Na+/K+-ATPase is a part of corneal endothelial cells, ciliary body, and iris, and its inhibition caused by exposure to bufadienolides induces corneal dysfunction, decreased vision, and ocular hypotonia. Effects of bufadienolides on the decrease of ocular pressure appear to be very strong, with quick action. This rarely described effect of the bufotoxin can be used as a basis for further research of toad venom and its pharmacological potential. Purpose. To present a case of a 67-year-old female patient who experienced a sudden decrease in vision after exposure to the poison from a common toad (Bufo bufo).

Development of a hybrid peptide dendrimer micellar carrier system and its application in the reformulation of a hydrophobic therapeutic agent derived from traditional Chinese medicine

A novel amphiphilic peptide dendrimer-based delivery system was developed for a cane toad poison-derived steroid. The methodology to incorporate lipid into asymmetric dendrimers generated self-assembled micelles.