| dc.contributor.author | Ivanitsa, A. O. | |
| dc.date.accessioned | 2025-11-28T16:19:56Z | |
| dc.date.available | 2025-11-28T16:19:56Z | |
| dc.date.issued | 2025 | |
| dc.identifier.citation | Ivanitsa A. O. PATHOPHYSIOLOGICAL MECHANISMS OF ACTION OF SNAKE VENOM / A. O. Ivanitsa // Перспективи та інновації науки (Серія «Педагогіка», Серія «Психологія», Серія «Медицина»). – 2025. – №10(56) - P. 2185 - 2193 | uk_UA |
| dc.identifier.other | https://doi.org/10.52058/2786-4952-2025-9(55)- | |
| dc.identifier.uri | https://dspace.vnmu.edu.ua/123456789/10754 | |
| dc.description.abstract | Snakebite is a major health issue worldwide, particularly affecting rural and tropical areas where medical facilities are scarce. Snake venom is a complex mixture of biologically active substances that can lead to serious hemostatic, neurotoxic and necrotic complications. The high mortality rate, particularly in South Asia and Africa, is the result of both strong venom toxicity and delayed treatment seeking by victims. The purpose of this review is to summarize the information on snake venom composition, its pathophysiological effect and situs actionis of active compounds. Materials and methods a search of literary resources in the Google Scholar, PubMed and Scopus data bases was made (30 publications were selected). Venom from snakes is a complex pool of biological substances consisting of enzymes (phospholipase A2, metalloproteinases, serine proteases), toxic proteins (cytotoxins, neurotoxins and cardiotoxins) and low molecular weight molecules which produce local or systemic reactions. Toxins easily get into the blood or lymph glands and half life of separate elements may be up to 10-60 hours. Cell membranes and necrosis are damaged, which lead to inflammation by PLA2 and cytotoxins. Vascular basement membrane is destroyed by metalloproteinases (notably class P-III), which results in hemorrhage, edema and microangiopathy. Neurotoxins and cardiotoxins competitively inhibit acetylcholine receptors or ion channels resulting in paralysis and arrhythmias. Similarly, serine proteases alter coagulation cascades usually resulting in thrombosis or consumptive coagulopathy. L-amino acid oxidases generate hydrogen peroxide, are toxic to cells and possess antimicrobial activity. Metalloproteinases also mediate the release of IL-1β, TNF-α and IL-6 in a process that activates the local inflammatory response. Snake venom is therefore a mixture of pathophysiologically active compounds with many toxins having multifunctional roles. Comprehensive study of the mechanisms of action of these animals provides an opportunity to perfect methods for treatment on intoxications and opens prospects for the development of new drugs. | uk_UA |
| dc.language.iso | en | uk_UA |
| dc.publisher | Перспективи та інновації науки (Серія «Педагогіка», Серія «Психологія», Серія «Медицина») | uk_UA |
| dc.relation.ispartofseries | 10;56 | |
| dc.subject | snake venom | uk_UA |
| dc.subject | pathophysiological mechanisms | uk_UA |
| dc.subject | neurotoxins | uk_UA |
| dc.subject | hemotoxins | uk_UA |
| dc.subject | coagulopathy | uk_UA |
| dc.title | PATHOPHYSIOLOGICAL MECHANISMS OF ACTION OF SNAKE VENOM | uk_UA |
| dc.type | Article | uk_UA |