Učinak piridostigmina i fizostigmina na akutnu toksičnost diizopropil fluorofosfata u štakora

Diisopropyl fluorophosphate (DFP) given to rats in lethal concentration (100 mg/m3, by inhalation for 40 min) significantly inhibited acetylcholinesterase activity in the blood, lung, liver and brain, and induced hyperglycaemia and glycogen mobilization in the liver, diaphragm and brain. Pretreatment (maximum sign-free dose) with carbamates, pyridostigmine (0.075 mg/kg, i.m.) or physostigmine (0.1 mg/kg, i.m.) 15 min before exposure to DFP, modified the inhibited acetylcholinesterase activity only in peripheral tissues. However, the hyperglycaemia and glycogen depletion induced by DFP inhalation were not modified by carbamate pretreatment. The time of survival of DFP exposed animals increased after pretreatment with carbamates, more after physostigmine (81 min) than after pyridostigmine (59 min). The animals exposed to DFP exhibited severe tremors and convulsions as compared to the animals pretreated with carbamates.Diizopropil fluorofosfat (DFP), koji su štakori primili u letalnoj koncentraciji (100 mg/m3) inhalacijom tijekom 40 minuta, značajno je inhibirao aktivnost acetilkolinesteraze u krvi, plućima, jetri i mozgu te izazvao hiperglikemiju i doveo do mobilizacije glikogena u jetri, dijafragmi i mozgu. Prethodno intramuskularno tretiranje životinja maksimalnom dozom karbarnata koja još ne izaziva znakove trovanja, i to piridostigminom (0,07.5 mg/kg) ili fizostigminom (0,1 mg/kg) petnaest minuta prije ekspozicije DFP-u dovelo je do promjene u inhibiciji aktivnosti acetilkolinesteraze samo u perifernim tkivima. Međutim, na hiperglikemiju i nedostatnost glikogena koji su bili izazvani inhaliranjem DFP-a prethodno tretiranje karbamatima nije utjecalo. Vrijeme preživljenja životinja koje su bile izložene DFP-u bilo je duže nakon što su životinje primile karbamate. U tom pogledu fizostigmin (81 min) je bio djelotvorniji od piridostigmina (59 minuta). U životinja koje su bile izložene DFP-u primijećeni su jači tremor i konvulzije nego u životinja koje su ranije bile tretirane karbarnatima

Treatment for Sulphur Mustard Poisoning -A Review

Sulphur mustard (SM) is a chemical warfare agent of historical and current interest It is a wellknown blistering agent or vesicant SM was extensively used in world war I as a chemical weaponand has been stockpiled by several counbies since that time. SM serves as an ideal war gas and is favoured militarily for its ability to incapacitate rather than to kill. Its use resulted in large numbers ofcasualties requiring prolonged and intensive medical care. Despite Geneva Protocol of 1925, which categorically bnned the production, stockpiling and use of chemical weapons in wars, SM has beenused in several wars, including the Iran-Irnq war during the 1980s, which renewed interest in it.Though, the chemical we'dpons convention was signed by more than 160 counbies in 1993 and wassubsequently ratified by several counbies, the threat from this agent persists due to its clandestineusage during war and also by teITOrist groups. There is no effective and specific antidote for local andsystemic toxicity of SM despite scientific research for more than 75 years. Many compounds weretested as antidotes for SM, but very few of them have been shown to provide some protection. The present review is aimed at evaluating the treatment regime and other clinical measures used to treat  SM victims and the various drugs and chemicals screened as antidotes for SM poisoning in experimental animals

Therapeutic Efficacy of Saline and Glucose Saline against Dermally applied Sulphur Mustard Intoxication in Mice

A single dose of saline or glucose-saline (5 mg glucose/kg) offered similar protection to mice against sulphur mustard intoxication, the extent of survival being 83 per cent as against 33 per cent without treatment. All the animals were protected when the treatment was extended by another two consecutive days in the glucose-saline treated group. Both saline and glucose-saline treatments could ameliorate the haemoconcentration as well as normalise pO/sub 2/ and % oxygen saturation. The protection conferred is attributed to the probable replenishment of fluid loss

Prophylactic Efficacy of Amifostine, DRDE-07, and their Analogues against Percutaneously Administered Nitrogen Mustards and Sulphur Mustard

Nitrogen mustards (HN-1, HN-2 and HN-3) and sulphur mustard are alkylating and blister-inducing chemical warfare agents. This study was aimed at investigating the prophylactic efficacy of amifostine, DRDE-07, and their analogues and some recommended antidotes against dermally-applied nitrogen mustards and sulphur mustard in preventing their systemic toxicity in mice. The antidotes were administered as single oral dose, 30 min prior to the mustard agent application. For DRDE-07, 0.2 LD50 (249 mg/kg) was used and for other analogues, equimolar dose of DRDE-07 was used. For amifostine, N-acetyl cysteine, melatonin and sodium thiosulphate, oral dose was 185 mg/kg, 250 mg/kg, 250 mg/kg, and 1000 mg/kg respectively. The animals were observed for mortality for 14 days. The protection index (PI) was calculated as a ratio of LD50 with treatment to LD50 without treatment. The protection of the antidotes was also determined by intraperitoneal route and half of the oral dose of the antidotes was given. The estimated percutaneous LD50 of HN-1, HN-2, HN-3 and sulphur mustard was 11.9 mg/kg, 20.0 mg/kg, 7.1 mg/kg and 7.1 mg/kg, respectively. Compounds that showed marginal protection against HN-1 were DRDE-10 and melatonin with a PI of 1.4. Compounds that showed marginal protection against HN-2 were amifostine, DRDE-07, DRDE-09, DRDE-30, DRDE-35 and melatonin with a PI of 1.4. Compounds that showed marginal protection against HN-3 were amifostine, DRDE-30, DRDE-35, sodium thiosulphate and melatonin with a PI of 1.7. In the case of sulphur mustard, DRDE-07, DRDE-10, DRDE-21, DRDE-30, and DRDE-35 gave a good protection with a PI of more than 5.0. Amifostine and sodium thiosulphate gave a PI of 4.5 and 4.0, respectively, while DRDE-09, N-acetyl cysteine and melatonin gave less protection against sulphur mustard. Intraperitoneally administered amifostine, DRDE-30, sodium thiosulphate and melatonin gave marginal protection against HN-2 with a PI of 1.2, while intraperitoneally administered amifostine, DRDE-07, DRDE-09, DRDE-10, DRDE-30, DRDE-35 and melatonin gave excellent protection against percutaneously administered sulphur mustard with a PI of more than 5.0. The present study shows, that oral and intraperitoneal administration of amifostine, DRDE-07 and their analogues are effective as prophylactic agents for sulphur mustard systemic toxicity, but not against nitrogen mustards.Defence Science Journal, 2009, 59(5), pp.512-516, DOI:http://dx.doi.org/10.14429/dsj.59.155

Clinical profile of a case of lumbar sacralisation- a naturopathy and physiotherapy management: case report

Lumbar sacralisation is a congenital anamoly, in which the transverse process of the last lumbar vertebrae (L5) fuses to the sacrum on one side (or) both (or) to ilium (or) both. They occur during the period of growth, grow away from spinal column and rarely responsible for mechanical symptoms and varies postural defect. This paper reports a rare presentation of deeper radiological structures of spine with mechanical instability, postural defect, mild to moderate pain in back and radiating towards left leg. Patient was 23 years old female and misdiagnosed as mechanical back pain and disc prolapsed. We assessed her clinically and radiologically and diagnosis was established based on X-rays and MRI of Spine. She was treated with integrated approach [naturopathy& physiotherapy] and patients recover uneventfully

A rare case report of massive ovarian edema

Massive ovarian oedema is a benign ovarian pathology occurs due to partial ovarian torsion and blockage of lymphatic drainage of the ovary. Commonly presents with pain abdomen on and off or abnormal uterine bleeding. Here we report a case of 15 years old girl with spotting per vaginum for 45 days. On examination, revealed 28 weeks size mass arising from pelvis. On further evaluation and blood works, proceeded with surgical management. Histopathological examination revealed benign massive ovarian oedema. However, it’s important to know differential diagnosis for solid ovarian tumours

Carbon Nanotubes: Detection of Chemical and Biological Warfare Agents

Discovery of carbon nanotubes has great impact on the development of newer methodologies and devicesuseful for the analysis of various types of chemicals. The functionalisation of CNTs with biomolecules relatedto chemical and biological warfare agents makes these useful for the detection of these agents. The detectionsensitivity can be increased manyfold. Various types of chemical and biological sensors were developed usingvarious type of carbon nanotubes as well as nano particles of different metals.Defence Science Journal, 2008, 58(5), pp.617-625, DOI:http://dx.doi.org/10.14429/dsj.58.168

Effect of Ricin on Some Biochemical, Haematological, and Histopathological Variables in Mice

Acute toxicity studies of ricin were carried out in Swiss albino male mice. The median lethal concentration (LD,,) values were determined for mice through intraperitoneal and oral routes and were found to be 1.01 ~ g l k gan d 28.29 mglkg, respectively. The ricin (1.0 LD,d was administered in mice through intraperitoneal route and various toxicity-related clinical var~ableswere studied on the I", 3'd, and the 7" day of post-exposure. The prominent symptoms before death, were diarrhoea with black sticky vent and piloerection. The body weight decreasedsignificantly in a dose-dependent manner. No significant change was observed in organ-to-body weight ratio on the 1". 3d, and the 7th day of post-exposure except kidney weight. On the 71h day, kidney weight increased significantty. The levels of bloodurea, uric acid, and glucose increased, while total protein level decreased. However, activities of transaminase and phosphatases were not altered. Leukocytosis was also observed. The ricin also affected blood coagulation parameters. There was a significant increase in the clotting time. However, prothrombin time, bleeding time, and erythrocyte sedimentation rate were not altered. Histopathological studies showed degenerative changes in various visceral organs, viz, lungs, liver, spleen, kidney, and testis. Acute toxicity studies of ricin revealed that it is a highly toxic toxin. The ricin intoxication caused alterations in biochemical, haematological variables, and degenerative changes in various visceral organs