RESUMEN
Increased resistance to a large number of antibacterial drugs poses a serious challenge in chemotheraphy of infectious diseases. Here, we have made and attempt to redesign the existing chemotherapeutic agent enrofloxacin (EN) to treat resistant bacteria. Precisely, we synthezied EN conjugated zinc oxide nanoparticles (EN-ZNP) and explored enhancing the antibacterial activity of enrofloxacin. Zinc oxide nanoparticles (ZNP) were synthesized by microwave irradiation and amine functionalization by co-condensation with APTES and then by utilizing EPC/NHS chemistry, enrofoxacin was conjugated. Conjugation and their stability were confirmed by FT-IR spectra and Zeta potential. EN fraction in EN-ZNP was determined indirectly using UV-Vis spectroscopy. The MIC values obtained for EN-ZNP against MTCC cultures and clinical isolates of Escherichia coli, Salmonella typhimurium, Staphylococcus aureus were significantly (P <0.05) lower than ZNP and, when compared to native EN it is significantly higher. However, the concentration of conjugated EN in EN-ZNP was significantly lower than the MIC of native EN. The results suggest that enrofloxacin can be successfully conjugated with amine functionalized zinc oxide nanoparticles. The antibacterial efficacy was significantly improved when ZNP conjugated with EN against standard MTCC cultures and clinical isolates.
RESUMEN
Administration of cadmium (Cd) significantly increased the peroxidation markers such as malondialdehyde and protein carbonyls along with significant decrease in antioxidant markers such as super oxide dismutase and reduced glutathione in liver and kidney tissues. Cadmium also caused a significant alteration in hepatic and renal functional markers in serum viz. total protein, albumin, alanine transaminase, blood urea nitrogen and creatinine. Prominent pathological changes observed in liver were severe vascular and sinusoidal congestion with diffuse degenerative changes and mononuclear infiltration into peripheral areas, while the kidney showed vascular and glomerular congestion, cloudy swelling of tubular epithelium. Co-administration of ethonolic extract of T. terrestris or vitamin E along with Cd significantly reversed the Cd induced changes along with significant reduction in Cd load.
RESUMEN
Cadmium (Cd) is a potential environmental pollutant and causes severe damage to reproductive organs in adults including ovary and testes. Of all antioxidants α-tocopheral is considered to be most potent chain breaking antioxidant. Our aim was to study the effect of α-tocopheral on biochemical and histological alterations induced by Cd in testes of rats. Group 1 served as control, while groups 2 and 3 received subcutaneous injections of CdCl2 (3 mg/kg b.wt) once a week for four weeks. Group 3 in addition received α-tocopheral (75 mg/kg b.wt.) orally, daily for six weeks. Cadmium caused testicular tissue biochemical alterations such as significant increase in MDA, a peroxidation marker, decrease in antioxidant markers viz SOD, CAT and GSH and functional markers viz ALP and LDH. Histological alteration induced by Cd consisted of desquamation of basal lamina, shrunken tubules, generalized germ cell depletion with multinucleated gaint cells, degenerating Leydig cells, vascular congestion, interstitial edema and significant reduction in spermatodynamic count. α- tocopheral significantly reversed all the Cd induced alterations. These results indicate that α-tocopheral has a protective effect against Cd indced biochemical and histological alterations in rat testes.
RESUMEN
To elucidate the role of acetylcholinesterase (AChE) enzyme in BBB function, phosalone, an organophosphorous compound, was studied using rat brain micro vessels in vitro. Phosalone at 100 mg/kg b. wt. induced convulsions and caused a significant inhibition of AChE resulting in increased permeability as assessed by volume distribution. The anaesthetized phosalone treated group also increased permeability as compared to the control but the values were significantly (P<0.05) lower than phosalone alone treated group. The inhibition of AChE enzyme has altered the barrier function at the dose level at which it caused convulsion and had an added effect on permeability of BBB.