Abstract This study evaluated the genotoxicity, mutagenicity, antigenotoxicity, and antimutagenicity effects on biochemical parameters of oxidative stress of the Spondias dulcis bark ethanolic extract on mice. The extract was evaluated in the doses of 500, 1000, and 1500 mg/kg bw via gavage. To evaluate the protective effects of the extract, benzo[a]pyrene (B[a]P) and cyclophosphamide (CP) were chosen as DNA damage inducers. Genotoxicity and antigenotoxicity were evaluated by the comet assay. Cytotoxicity, mutagenicity, and antimutagenicity were evaluated by the micronucleus test in bone marrow and peripheral blood. The biochemical parameters of oxidative stress were evaluated by the quantification of catalase activity (CAT) and reduced glutathione (GSH) in total blood, liver and kidney, and malondialdehyde (MDA), in liver and kidney. No genotoxic, cytotoxic, or mutagenic effect was found on mice exposed to the extract. The extract depleted the number of damaged nucleoids in total blood and the number of micronucleus (MN) in both cell types. The extract was able to increase CAT activity and GSH levels and decrease MDA levels after treatment with B[a]P and CP. The results indicate that the S. dulcis extract has potential to be used as preventive compound against DNA damage caused by CP and B[a]P.

Cardioleputin, a new cardioactive toxin, was purified from a stonefish venom using column chromatographies. The purified toxin was found to be an unstable protein that was susceptible to heat and freeze-thawing. This protein showed to have a molecular size of 46,000 daltons, and its amino acid composition was rich in serine and glycine, but low in basic amino acids. The crude venom induced a sudden drop in blood pressure and heart rate of rats right after administration. Both the blood pressure and heart rate returned to their original values as time elapsed, and thereafter continued to show a gradual decrease. In addition, crude venom actively affected the contractile response and suppressed the heart rate of guinea pig atria. The purified toxin caused irreversible inotropical and chronotropical increases in guinea pig atria. The action of the toxin on the atria was completely different from that of lysolecithin. It might be suggested that the toxin acts on the Ca<img SRC="http:/img/fbpe/jvat/v2n2/image2184.gif"> ion channel of the atrial membrane.