Characterization of biological activity of Scatophagus argus venom.
Scatophagus argus of the family Scatophagidae inflicts painful wounds in fishermen while handling it. The venom induces prominent local tissue damage characterized by pain, edema and necrosis. The pathogenesis of acute muscle damage in gastrocnemius muscle induced by S. argus venom was studied in mice. The inflammatory response induced by S. argus venom in the mice hind paw was studied measuring paw edema. Intramuscular injection of S. argus venom induced motoxicity. The effect of S. argus venom on the cellular components of inflammatory response was investigated. Venom from S. argus were quantitatively analyzed for enzymic and biochemical activity. The biochemical changes induced by the sublethal concentration of S. argus venom and histopathological studies of effect of venom on mice were carried out. Venom induced a rapid increment in serum creatine kinase (CK) and lactate dehydrogenase (LDH) showing the myotoxicity of venom. Concomitant with this a reduction of muscle CK and LDH activity was observed, where as no increment in muscle lactate was detected. Our findings showed that the edematic activity was dose dependent and remained significantly elevated over 48 h after injection. Administration of S. argus venom caused a significant cell accumulation of neutrophils in to peritoneal cavity as well as foot pad up to 24h with maximal being at 4-6h. The venom components analyzed showed the presence of phosphodiesterase, acid phosphatases, alkaline phosphatases, proteinase, and caseinolytic activity. SDS PAGE revealed the presence of major and minor protein bands between 6.5 and 68 kDa. The biochemical changes induced by the sublethal concentration of S. argus venom showed reversible changes in the hematological (blood cell count, hematocrit, hemoglobin, mean corpuscular volume, mean corpuscular hemoglobin and platelet count) parameters which were significantly altered at 6 and 24h (GLM repeated measures p<0.05). Serum enzymes such as AST, ALT, ACP, ALP, LDH and urea were altered significantly which in turn confirmed the damage of vital organ tissue.
Sivan
Gisha
G
Department of Marine Biology, Microbiology and Biochemistry, Cochin University of Science and Technology, Kochi 682016, Kerala, India. gishasivan@rediffmail.com
Venketasvaran
K
K
Radhakrishnan
C K
CK
D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000201:enzymology; D002465:Cell Movement / Q000187:drug effects; D003402:Creatine Kinase / Q000097:blood; D004487:Edema / Q000139:chemically induced / Q000473:pathology; D005397:Fish Venoms / Q000737:chemistry* / Q000633:toxicity; D005528:Foot; D006614:Hindlimb; D007249:Inflammation / Q000097:blood / Q000139:chemically induced* / Q000473:pathology; D007273:Injections, Intramuscular; D007274:Injections, Intraperitoneal; D007770:L-Lactate Dehydrogenase / Q000097:blood; D007962:Leukocytes / Q000187:drug effects; D008297:Male; D051379:Mice; D009043:Motor Activity / Q000187:drug effects; D018482:Muscle, Skeletal / Q000187:drug effects / Q000201:enzymology / Q000502:physiology; D009504:Neutrophils / Q000187:drug effects; D010473:Perciformes / Q000502:physiology*; D010538:Peritonitis / Q000139:chemically induced / Q000473:pathology
D005397:Fish Venoms; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase; D000110:Acetylcholinesterase