الفهرس 
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Abstract
Marine predatory cone snails develop a complicated mixture of conotoxins and conopeptides as powerful weapons for hunting, defending and deterring competitors. These bioactive peptides are hypervariable and active on a number of ion channels or receptors. Cytotoxic effects of venom from the marine cone snail Conus flavidus were recorded to know its effect, toxicity and to reveal the mechanism of action.
To characterize the venom properties we record its effect on mammalian tissue on different periodic times were assessed for the main organs liver and heart. Also its antibacterial effect was recorded to determine its antibacterial assays on different strains of bacteria and its minimum inhibitory concentration was obtained.
To evaluate variability in cytotoxic effect of Conus flavidus crude venom the ½ LC50 (8.23 µg/ml) of the crude venom was injected intraperitoneally into adult male albino mice at six group (one control and five treated groups). The oxidative stress biomarkers (lipid peroxidation (MDA), protein carbonyl content (PCC), non-enzymatic (levels of blood and liver glutathione reduced form (GSH), nitric oxide (NO)) and enzymatic antioxidants (superoxide dismutase (Cu/Zn-SOD), catalase (CAT)), as well as the total antioxidant capacity (TAC) were measured 2,4, 6, 12 and 24 h., post venom injection.
All the tested biochemical parameters revealed significant differences in toxicity in venom taken from the different populations. The results showed that the venom induced significant increase (P<0.05) in the level of PCC, MDA, NO, GSH and the activity of CAT. On the other hand, the venoms inhibited significantly (P<0.05) the activity of Cu/Zn SOD and the total antioxidant capacity.
Also its effect on mammalian tissue was studied as two main organs heart and liver, the venom show different changes on liver tissue including cytoplasmic degeneration, lymphatic aggregation, hepatocytes degeneration and sinusoidal congestion, the heart tissue also showed degeneration myofibrils, edema, congested blood vessels and hemorrhage. The changes at both liver and heart increased with time passing.
Using six bacterial strains, the venom showed activity against five strains with maximum inhibition zone in Enterococcus faecalis and minimum inhibition zone in Streptococcus pyogenes, and no activity was recorded against Pseudomonas aeruginosa. Resistance arises as a consequence of mutations in microbes and selection pressure from antibiotic use that provides a competitive advantage for mutated strains.