Učinak nekih lijekova na glikogen i nivo acetilkolina u tkivu mozga i perifernim tkivima u štakora s hiperglikemijom izazvanom malationom

The hyperglycaemia induced by malathion (5OO mg/kg, i.p.) in rats was accompanied by depletion of glycogen in certain brain regions and peripheral tissues and an increase in the level of cortical and striatal acetylcholine. Thn induced changes were abolished by pralidoxime (100 mg/kg, i.p.) given immediately after malathion, but persisted when oxime was given 30 min after malathion treatment. Atropine (25 mg/kg, i.p.) prevented the malathion induced hyperglycaemia and changes in the level of glycogen. The cortical and striatal acetylcholine levels in these animals were significantly higher than in controls. Pretreatment with reserpine (1.0 mg/kg, i.p.) daily for three days did not modify the malathion induced changes in the levels of blood glucose, glycogen and acetylcholine. The increased acetylcholine level in the brain may have been related to changes in the level of glycogen and blood glucose in malathion treated animals.Ustanovljeno je da hirperglikemiju u štakora izazvanu malationom (500 mg/kg, i. p.) prati nestanak glikogena u nekim područjima mozga i perifernim tkivima i porast acetilkolina u kortikalnom i strijatalnom dijelu mozga. Ove promjene nestale su kad je odmah nakon malationa dan pralidoksim (100 mg/kg, i. p.), ali su se zadržale kad je oksim dan 30 minuta nakon malationa. Atropin (25 mg/kg, i. p.) je spriječio hiperglikemiju izazvanu malationom i promjene u nivou glikogena. Nivo acetilkolina u kortikalnom i strijatalnom dijelu mozga bio je značajno viši u tretiranih životinja nego u kontrolnih. Prethodni trodnevni tretman rezerpinom (1,0 mg/kg dnevno, i. p.) nije utjecao na promjene koje je izazvao malation u nivou glukoze u krvi, glikogena i acetilkolina. Povišene vrijednosti acetilkolina u mozgu mogu se dovesti u vezu s promjenama u nivou glikogena i glukoze u krvi životinja tretiranih rnalationom

Uloga adrenalnih žlijezda u nastanku promjena u metabolizmu ugljikohidrata izazvanih diazinonom u štakora

Treatment of rats with diazinon (40 mg/kg, i.p.) resulted in hyper-glycaemia and depletion of glycogen from the brain and peripheral tissues two hours after administration. The activities of glycogen phosphorylase and phosphoglucomutase were significantly higher in the brain and liver; that of glucose-6-phosphatase was not altered. The activities of the glycolytic enzymes hexokinase and lactate dehydrogenase were increased only in the brain. The cholinesterase activity in the brain was reduced by treatment with diazinon. The activities of the hepatic gluconeogenic enzymes fructose I.6-diphosphatase and phosphoenolpyruvate carboxykinase were significantly increased. The lactate level was increased in the brain and blood, whereas that of pyruvate was not changed. The activity of glucose-6-phosphate dehydrogenase was not changed to any major extent. Cholesterol and ascorbic acid contents of adrenals were depleted in diazinon-treated animals. The changes were pronounced after intraperitoneal administration of 40 mg/kg diazinon, they were slight but significant after 20 mg/kg, and absent after l0 mg/kg. Hyperglycaemia and changes in carbohydrate metabolism were abolished by adrenalectomy suggesting possible involvement of adrenals.U štakora koji su dobivali diazinon (40 mg/kg) intraperitonealno dva sata nakon pnm1ene utvrđena je hiperglikemija i smanjenje nivoa glikogena u tkivima mozga i živaca. Aktivnosti glikogen fosforilaze i fosfoglukomutaze u mozgu i jetri bile su značajno više, dok se aktivnost glukoza-6-fosfataze nije promijenila. Glikolitski enzimi heksokinaza i laktat dehidrogenaza imali su povišenu aktivnost samo u mozgu. Tretman diazinonom doveo je do smanjene aktivnosti kolinesteraze u mozgu. Aktivnosti glukoneogenih enzima jetre fruktoza 1,6-difosfataze i fosfoenolpiruvatne karboksikinaze značajno su porasle. Nivo laktata bio je povišen u mozgu i krvi, dok je koncentracija piruvata ostala nepromijenjena. Aktivnost glukoza-6-fosfatne dehidrogenaze nije se bitno promijenila. Sadržaj kolesterola i askorbinske kiseline u nadbubrežnim žlijezdama bioje niži u životinja koje su primale diazinon, Promjene su bile najizraženije nakon doze od 40 mg kg diazinona, male ali značajne nakon doze od 20 mg/kg, a nije ih bilo nakon doze od 10 mg/kg. Hiperglikemija i promjene u metabolizmu ugljikohidrata bile su spriječene adrenalektomijom što ukazuje na moguću ulogu nadbubrežnih žlijezda u biokemijskim promjenama izazvanima diazinonom

Glikoliza i glikogenoliza u mozgu životinja tretiranih diazinonom

Treatment with diazinon (40 mg/kg, i. p.) resulted in depletion of glycogen and increased activities of glycogen phosphorylase, phosphoglucomutase, hexokinase and lactate dehydrogenase in the brain of rats. The activity of glucose-o-phosphatase was not significantly changed. The level of lactic acid in the blood was raised, while that of pyruvic was not altered. The induced changes may be due to a compensatory mechanism providing extra energy on account of stimulatory effects in diazinon treated animals.Davanje diazinona (40 mg/kg i. p.) imalo je za posljedicu iscrpljenje glikogena u mozgu štakora te povećanu aktivnost glikogen fosforilaze, fosfoglukomutaze, heksokinaze i laktat dehidrogenaze. Aktivnost glukoza-6-fosfataze nije bila značajnije promijenjena. Razina mliječne kiseline u krvi bila je povećana, dok se koncentracija pirogrožđane kiseline nije mijenjala. Ove inducirane promjene mogu biti posljedica kompenzacijskog mehanizma da bi se stvorila dodatna energija kao posljedica stimulatornih učinaka diazinona u trovanih životinja

Učinak nekih lijekova na glikogen i nivo acetilkolina u tkivu mozga i perifernim tkivima u štakora s hiperglikemijom izazvanom malationom

The hyperglycaemia induced by malathion (500 mg/kg, I.p.) i1ll rats was accompanied by depletion of glycogen in certain brain regions and peripheral tissues and an increase in the level of cortical and striatal acetylcholine. The induced changes were abolished by pralidoxime (100 mg/kg, i.p.) given immediately after malathion, but persisted when oxime was given 30 min after malathion treatment. Atropine (25 mg/kg, i.p.) prevented the malathion induced hyperglycaemia and changes in the level of glycogen. The cortical and striatal acetylcholine levels in these animals were significantly higher than in controls. Pretreatment with reserpine (1.0 mg/kg, i.p.) daily for three days did not modify the malathion induced changes in the levels of blood glucose, glycogen and acetylcholine. The increased acetylcho1ine level in the brain may have been related to changes in the level of glycogen and blood glucose in malathion treated animalsUstanovljeno je da hiperglikemiju u štakora izazvanu malationom (500 mg/kg, i. p.) prati nestanak glikogena u nekim područjima mozga i perifernim tkivima i porast acetilkolina u kortikalnom i 1strijatalnom .dijelu mozga. Ove promjene nestale su kad je odmah nakon malationa dan pralidoksim (100 mg/kg, i. p.), ali su se zadržale kad je oksim dan 30 minuta nakon malationa. Atropin (25 mg/kg, i. p.) je spriječio hiperglikerniju izazvanu malationom i promjene u nivou glikogena. Nivo acetilkolina u kortikalnom i strijatalnom dijelu mozga bio je značajno viši u tretiranih životinja nego u kontrolnih. Prethodni trodnevni tretman rezerpinorn (1,0 mg/kg dnevno, i. p.) nije utjecao na promjene koje je izazvao malation u nivou glukoze u krvi glikogena i acetilkolina. Povišene vrijednosti acetilkolina u mozgu mogu se dovesti u vezu s promjenama u nivou glikogena i glukoze u krvi životinja tretiranih rnalationom

Multiple stochastic pathways in forced peptide-lipid membrane detachment

We have used high resolution AFM based dynamic force spectroscopy to investigate peptide-lipid membrane interactions by measuring the detachment (last-rupture) force distribution, P(F), and the corresponding force dependent rupture rate, k(F), for two different peptides and lipid bilayers. The measured quantities, which differed considerably for different peptides, lipid-membranes, AFM tips (prepared under identical conditions), and retraction speeds of the AFM cantilever, could not be described in terms of the standard theory, according to which detachment occurs along a single pathway, corresponding to a diffusive escape process across a free energy barrier. In particular, the prominent retraction speed dependence of k(F) was a clear indication that peptide-lipid membrane dissociation occurs stochastically along several detachment pathways. Thereby, we have formulated a general theoretical approach for describing P(F) and k(F), by assuming that peptide detachment from lipid membranes occurs, with certain probability, along a few dominant diffusive pathways. This new method was validated through a consistent interpretation of the experimental data. Furthermore, we have found that for moderate retraction speeds at intermediate force values, k(F) exhibits catch-bond behavior (i.e. decreasing detachment rate with increasing force). According to the proposed model this behavior is due to the stochastic mixing of individual detachment pathways which do not convert or cross during rupture. To our knowledge, such catch-bond mechanism has not been proposed and demonstrated before for a peptide-lipid interaction