Troponin-I, homocysteine, Creatine kinase-myocardial band, lactate dehydrogenase and acute phase response had been evaluated in calves with myocarditis due to FMD. The study was conducted on 52 local breed calves 1-6 months old and from both sexes, their dams have no history for vaccination against FMD and show classical foot and mouth disease signs. Ten clinically healthy calves of the same ages were considered as controls. Suspected calves neither show oral blisters, rope salivation, nor foot lesions. Diseased calves showed signs of dullness, in activity, panting with mouth breathing, unable to suck, recumbency, However, five of diseased calves were died within 24-72 hours and on macroscopic examinations of autopsied animals, necrotic myocarditis with pale foci with a zone of hyperemia which were present on the papillary and ventricular cardiac muscles, moreover, on histopathological examinations there were severe inflammatory cells infiltration in the interstitial of myocardial fibers with obvious area of coagulation of myocardial fibers and marked area of hyalinization, furthermore, severe mononuclear cells infiltration, mainly lymphocytes, with few neutrophils closed to necrotic myocardial fibers were also detected. Diagnosis of FMD virus was confirmed by using commercially NSP ELISA kits for foot and mouth. A significant increase (p<0.05) was encountered in body temperature, respiratory and heart rates in diseased animals than in controls, Furthermore, abnormal cardiac sounds (organic murmurs) were indicated on auscultation of the heart. Results of hematological parameters shown a significant increase indicated in ESR values of diseased calves than in controls, moreover, total leukocyte count was increased significantly with significant lymphocytosis. Furthermore, the results were also showed significant increase in values of serum cardiac troponin, homocysteine, creatine kinase-myocardial band, lactate dehydrogenase, haptoglobin and fibrinogen in seropositive calves for FMD compared with controls. It can be concluded that determination of cardiac biomarkers and acute phase response concentration in calves with myocarditis can considered as a guide to quantify early heart damage.
Acute enzootic muscular dystrophy of adult lambs due to vitamin E and/or selenium deficiency was suspected in local adult lambs of Basrah, Iraq. The study was conducted on 82 adults local breed lambs 8-11 months of age. Suspected animals show panting with increase abdominal respiration and mouth breathing, recumbence and unable to stand with acute death within 24-48 h. Fifteen clinically healthy lambs were considered as controls. The hematological changes indicated a significant decrease in RBC, Hb, and PCV reflected macrocytic hypochromic type of anemia. Indices of clotting factors show significant changes in diseased adult lambs. Results of the biochemical changes indicated a significant decrease of vitamin E, and the glutathione peroxidase, in diseased animals, whereas, a significant increase indicated in the values of AST, CK and troponin I. Results of the post-mortem examinations showed enlargement of the heart with a white-colored irregular patch. Furthermore, results of histopathological changes indicated an acute cellular degeneration of myocardial fibers associated with diffuse interstitial edematous fluid in the myocardial parenchyma and acute cellular degenerative myocardial fibers with a marked degree of degeneration in the myocardial parenchyma. It has been concluded that, acute enzootic muscular dystrophy has an adverse harmful clinical effect on adult diseased lambs which could always be terminated with death.
In order to estimate the ameliorating effects of alpha lipoic acid (ALA) on the nephropathy of diabetes mellitus (DM) associated with oxidative stress, this study performed in 18 adults male rabbits were divided into 3 equal groups, the group-I was regard as control while group-II Induced DM only by intravenously single dose (150 mg/kg b.w.) of alloxan-monohydrate; group-III was induced DM by intravenously single dose of (150mg/kg b.w.) of alloxan-monohydrate and then treated by (10mg/kg b.w.) daily of ALA intraperitoneally for 4 weeks. The biochemical results showed significant (P≤0.05) decreased of the serum values of GSH, CAT and SOD as well, significantly (P≤0.05) increased of MDA, peroxynitrate, creatinine and BUN of group-II when compared to control; also the result of group-III showed nonsignificant (P˃0.05) differences of GSH, SOD, MDA, creatinine, BUN and peroxynitrate when compared to control. The histopathological and histochemical results of kidney of group-II showed moderate thickness of basement membrane of glomeruli with compressed capillaries as well infiltration of glyco-proteinaceous materials in glomeruli and around renal tubules with some vacuolation of these tubules and mesangial cells; while the results of group-III showed normal architectures with very mild degree of vacuolation of few renal tubules in addition to disappearance of glyco-proteinaceous materials in this group; in conclusion, ALA had a dual protective effects on nephropathy by scavenging the oxidative stress free radicals and enhanced insulin metabolism.
T HE protective role of Vit.B 12 on neurotoxic effect of diazinon has been studied and conducted on 24 adults male wistar rats were divided equally into 4 groups, the group I was used as normal control; group II was orally given 1/10 LD 50 (3.8mg/kg.bw) of diazinon for one month; group III was orally given 1/10 LD 50 (3.8mg/kg.bw) of diazinon plus systemic injection (I.M route) of Vit.B 12 (4 mg/kg.bw) for one month; group IV was given systemic injection (I.M route) of Vit.B 12 (4 mg/kg.bw) only for one month. Biochemically it revealed a significant (P≤0.05) increase in GSH, CAT and SOD values in both Vit.B 12 groups (group III and group IV) as well to control group when compared to diazinon group (group II); while the values of MDA and peroxynitrite revealed a significant (P≤0.05) decreases in the both Vit.B 12 groups (group III and group IV) as well to control group when compared to diazinon group (group II); moreover, the histopathological results of the diazinon group (group II) revealed a serious neurologic changes included necrotized neurons, diffuse neuronal edema, perivascular edema and hyperplasia of glial cells; while the Vit.B 12 groups showed no effective histopathological changes were more or less to control group. There are a little information has been provided concerning the relation between diazinon and Vit.B 12 ,therefore, the current study concluded that the Vit.B 12 has a significant protective role against the neurological toxic effects of diazinon on basis of histopathological and biochemical patterns.
In order to determine the genotoxic effects of diazinon and the role of chitosan to neutralize these effects, our study performed in (24) male rats (Rattus norvegicus) were divided into four groups and treated for (60) days as following, group (A) treated with normal saline and served as control, group (B) treated with [(1/10LD50) 3.8mg/kg. bw] of diazinon, group (C) treated with [(1/10LD50) 3.8mg/kg. bw] of diazinon and fed on diet supplement containing (1gram/1kg ration) chitosan, group (D) fed on diet supplement containing (1gram/1kg ration) chitosan only. The genotoxiceffect of diazinon was evaluated by using the micronucleus assay showed increasing of micronucleated polychromatic erythrocytes were (11.6%) in group B, while (7%) in group C . The chromosomal aberration showed increase of presence of chromosomal aberration in group B was (7.5±1.04), while in the group C showed mild elevation in (3.25±0.8). The polymorphism of GSTM1 and GSTT1 genes showed highly incidence of both genes polymorphism in group B was (66.6%) while group C was (50%) . we concluded that diazinon is genotoxic pesticide and chitosan ameliorate it effects.
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