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S. Suchalatha C. S. Shyamala Devi 《Indian journal of clinical biochemistry : IJCB》2004,19(2):184-189
To study the protective role of Arogh on isoproterenol induced myocardial damage in rats. The effect of Arogh pretreatment
on isoproterenol induced myocardial damage was assessed by studying the levels of lipid peroxides and changes in the activity
of marker enzymes such as creatine kinase, lactate dehydrogenase and transaminases in serum and heart tissue. In isoproterenol
administered rats, a significant decrease was observed in the activity of marker enzymes in the heart with a corresponding
increase in their levels in serum. Lipid peroxide levels increased significantly in the serum and heart. In rats pretreated
with arogh, the level of lipid peroxides and the activity of marker enzymes were maintained at near normal values. Pretreatment
with Arogh offered a protective effect against isoproterenol induced myocardial damage in rats as evidenced by LDH isoenzyme
patterm and histopathological studies of heart tissue. 相似文献
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J Kato Alice Abraham Ruram S Sekharjit Singh S Bilasini Devi Th Ibetombi Devi W Gyaneshwar Singh 《Indian journal of clinical biochemistry : IJCB》2007,22(1):128-130
The present, study was conducted to determine the level of malondialdehyde (MDA) as an index of free radial induced lipid
peroxidation and antioxidant vitamins-vitamins A, vitamin C and vitamin E in 75 confirmed cases of urolithiasis. Significantly
high level of MDA (p<0.001) with significantly low levels of vitamin E (p<0.001) and vitamin A (p<0.001) with no significant
decrease in vitamin C (p>0.05) were observed in the plasma of urolithiasis cases as compared to normal controls. In conclusion,
it appears that a role of lipid peroxidation and oxidative function exists in the pathogenesis of urolithiasis. But, the exact
mechanism how this occurs remains to be elucidated. 相似文献
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Thyagaraju K. Hemavathi B. Vasundhara K. Rao A. D. Devi K. N. 《Journal of Zhejiang University. Science. B》2005,6(8):759-769
A comparative study was made on the tissue specific expression of glutathione transferases (GST) in brain and testis after
exposure of rat to phenobarbitol (PB) and β-methylcholanthrene (MC). Glutathione transferases, a family of multifunctional
proteins are involved in intracellular transport processes and in detoxication of electrophilic xenobiotics by catalyzing
reactions such as conjugation, isomerization, reduction and thiolysis. On purification, the yield of GST proteins by affinity
chromatography was 39% in testis and 32% in brain. The affinity purified testis GSTs were resolved by chromatofocusing into
six anionic and four cationic isozymes, and in brain glutathione transferases were resolved into four anionic and three cationic
isozymes, suggesting the presence of multiple isozymes with Yc, Yb, Yβ and Yδ in both of them. In testis and brain, these
isozymes at identical pI values showed variable functions with a battery of substrates and the cationic isozymes of brain
and testis showed identical properties in CHP (cumene hydroperoxide) at pH values of above 7.0. Substrate specificity studies
and immunoblot analysis of testis and brain proteins revealed that they play a predominant role in the detoxication of phenobarbitol
or β-methylcholanthrene. Expression of the isozymes in testis and brain on exposure to PB and MC indicated elevated subunit
variation. In both testis and brain, Yδ of π class was expressed on PB treatment and Yc of α class and Yβ of μ class was expressed
in MC treated testis and only Yc was predominantly expressed in MC treated brain. Thus these subunits expression is considered
as markers for carcinogenesis and specific to chemical toxicity under phenobarbitol and β-methylcholanthrene stress.
Project supported by Department of Science and Technology and Council for Scientific and Industrial Research, New Delhi 相似文献
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Anita Devi Ritu Singh Rajni Dawar Sanjay Tyagi 《Indian journal of clinical biochemistry : IJCB》2017,32(2):235-238
Association of cholesteryl ester transfer protein (CETP) Gene -629C/A Polymorphism with angiographically proven atherosclerosis CETP gene has been linked to CAD risk via its role in HDL and LDL metabolism. There is no agreement of whether CETP is atherogenic or not. Furthermore, various genotypes of CETP gene have been associated with CETP levels and thus with atherosclerosis risk. Our aim was to study the association of CETP -629C/A gene polymorphism with CETP and HDL levels and their association if any with atherosclerosis. Study population consisted of angiographically documented 50 cases with coronary artery atherosclerosis and 50 controls negative for atherosclerosis of coronary artery. Serum lipid profile was measured on SYNCHRON CX-9 using standard kits. Serum CETP levels were measured by ELISA method. CETP -629C/A gene polymorphism was studied using PCR–RFLP method. There was no significant difference in lipid profile of the two groups. However, serum CETP level was significantly higher (46.44 ± 21.75 ng/ml) in cases than controls (37.10 ± 21.92 ng/ml) with p value =0.035. The frequency of -629A allele was higher (0.85) in cases than that of controls (0.81). Homozygosity of A allele was more in subjects with atherosclerosis of coronary artery. We conclude that CETP is atherogenic and could be used as atherogenic risk predictor in angiographically proven atherosclerosis. Also A allele of -629C/A polymorphism is more prevalent in cases; indicating its effect on expression of CETP gene. 相似文献
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Serum glycoproteins were evaluated in oral squamous cell carcinoma patients treated with radiotherapy and also the effect
of vitamin E was studied. Cell surface glycoconjugates are important parameters in the detection of malignancy. Thus, the
objective of the present study is to evaluate the efficacy of vitamin E on glycoproteins in oral cavity cancer patients treated
with radiotherapy. The study includes 26 age and sex matched normal healthy individuals and 26 patients with squamous cell
carcinoma of oral cavity. These patients were divided into two groups, one for radiotherapy alone (at a dosage of 6000 cGy
in five fractions per week for a period of six weeks) and the other for radiotherapy plus vitamin E supplementation (at a
dosage of 400 IU / day of vitamin E) for the entire period of radiotherapy. Levels of hexose, hexosamine, fucose and sialic
acid were increased in oral squamous cell carcinoma patients and a significant decrease was observed in radiation treated
patients when compared to control. The levels of glycoconjugates were significantly decreased in radiation treated patients
supplemented with vitamin E. This measurement may be useful in assessing disease progression and identifying patients resistant
to therapy and a possible role of vitamin E on reduction in glycoconjugate levels of radiation treated oral squamous cell
carcinoma patients. 相似文献
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Prasanthi Mannava Afshan Masood Ambika K. Devi 《Indian journal of clinical biochemistry : IJCB》2015,30(1):113-116
Albright hereditary osteodystrophy (AHO) is a rare hereditary metabolic disorder that may or may not be associated with resistance to parathyroid hormone (pseudohypoparathyroidism) or other hormones. The disorder is commonly characterized by a constellation of dysmorphic physical features and with biochemical levels that demonstrate hypocalcaemia and hyperphosphatemia. We report here a clinical case of a 14 year old male with AHO and we discuss his clinical features, radiographic and laboratory findings along with treatment. 相似文献
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Angom Ranjana Devi Mahuya Sengupta Dipu Mani Barman Yashmin Choudhury 《Indian journal of clinical biochemistry : IJCB》2021,36(3):296
Nicotine, responsible for the addictive properties of tobacco, is widely used in nicotine replacement therapy for tobacco use cessation. We investigated the time-dependent effect of treatment with nicotine on the tumor suppressor, DNA repair and immune responses. Swiss Albino mice (laca strain) of both sexes received nicotine dissolved at a dose of 100 µg/ml in 2% sucrose for 24 weeks, by oral gavage, while age- and gender-matched controls received only 2% sucrose for the same period. Nicotine-treated and control mice were sacrificed 6, 16 and 24 weeks post-treatment, and their tissues evaluated for alterations in histology, oxidative stress, TNF-α levels, nitric oxide (NO) and myeloperoxidase (MPO) release, tumor suppressor response and DNA repair response. Statistical significance of results was determined using Students’ t test. The tissues of nicotine treated mice exhibited a large number of multinucleated and binucleated cells, enlarged nuclei and non-uniform distribution of cells, significant increase in expression of TNF-α gene and serum TNF-α, and time-dependent significant increase in lipid peroxidation, protein carbonylation, NO and MPO release when compared to age-and gender-matched controls. The mRNA expression of the tumor suppressor gene p53, its primary regulator Mdm2, and the DNA repair genes Brca2 and Ape1 were significantly elevated, but the corresponding protein levels remained largely unaltered. In conclusion, treatment with nicotine caused oxidative stress and inflammation which can cause widespread cellular damage from the very onset of treatment, without subverting the tumor suppressor and DNA repair responses.Electronic supplementary materialThe online version of this article (10.1007/s12291-020-00903-8) contains supplementary material, which is available to authorized users. 相似文献