ABSTRACT
Cataract, the lens opacity, is among major causes of blindness in Pakistani population. In recent past, oxidative stress is suggested to play crucial role in loss of transparency. Along with other antioxidants, Paraoxonase 1 [PON1] has also shown decreased activity in patients suffering from cataract. The aim of current study was to examine the possible association of PON polymorphism with predisposition of cataract formation in local population. The study was conducted on 51 cataract patients and 50 control subjects considering all ethical issues. DNA was extracted from whole blood and PON1 polymorphism was identified using tetra primer ARMS-PCR method for both positions L55M and Q192R. Tetra primer ARMS-PCR results revealed that association between L55M polymorphism and cataract was insignificant while 192R genotype PON1 frequency was higher among the people suffering from cataract [78.4%] as compared to control subjects [56%], [odds ratio=2.857, confidence interval=1.197-6.820]. Hence, R allele is likely to be a risk factor for cataract with allele frequency [82.3%] and [odds ratio=4.552, confidence interval=1.716-12.073, p-value=0.002]. PON1 Q192R polymorphism is likely to be a risk factor for cataract development in Pakistani population while PON1 L55M was not found to be associated with cataract
ABSTRACT
To complement an earlier analysis of protein alterations in plasma from uremic versus healthy subjects by addition of further LC-MS/MS analysis to the previously used MALDI-TOF mass analyses. Sequence identifications of tryptic peptides from SDS gel electrophoretic fractions of immunodepleted and HPLC-fractionated plasma was performed from seven chronic kidney disease stage 5 patients [age 55 +/- 14 years, glomerular filtration rate 6.9 +/- 2.9 mL/minute/1.73 m[2]] and from seven matched controls. About twice as many proteins were increased in uremic plasma as the previously identified. The identifications included proteins that consistently complement the two identification patterns regarding separate subunits from the same protein complex. Mass spectrometric analysis is applicable to complex plasma proteomes in clinical settings. The LC-MS/MS technique, based on individual peptide sequence analyses, gives increased identifications and also demonstrates feasibility of this technique in clinical practice
ABSTRACT
Tryptophan 2, 3-dioxygenase [TDO] a heme containing enzyme found in mammalian liver is responsible for tryptophan [Trp] catabolism. Tip is an essential amino acid that is degraded in to N-formylkynurenine by the action of TDO
The protein ligand interaction plays a significant role in structural based drug designing. The current study illustrates the binding of established antidepressants [Ads] against TDO enzyme using in-silico docking studies. For this purpose, Fluoxetine, Paroxetine, Sertraline, Fluvoxamine, Seproxetine, Citalopram, Moclobamide, Hyperforin and Amoxepine were selected. In-silico docking studies were carried out using Molegro Virtual Docker [MVD] software. Docking results show that all ADs fit well in the active site of TDO moreover Hyperforin and Paroxetine exhibited high docking scores of-152.484k cal/mol and -139.706k cal/mol, respectively. It is concluded that Hyperforin and Paroxetine are possible lead molecules because of their high docking scores as compared to other ADs examined. Therefore, these two ADs stand as potent inhibitors of TDO enzyme
ABSTRACT
The possibility that monoamine deficiency in brain is the basis of schizophrenia was investigated. The brains from rabbits, after injection of serum from Schizophrenic patients, were determined spectroflourimetrically for their content of tryptophan, 5-hydroxytryptamine [5-HT] and 5-hydroxyindole acetic acid [5H1AA] and compared with appropriate controls 5-HT content was significantly decreased in the region of hypothalamus and cerebellum [P < 0.01]. The content of 5-H1AA in the region of cortex, mid-brain and hypothalamus was also low [P < 0.01]. Whereas, tryptophan content was not found to be significantly different between schizophrenics and control