Krishnamurti Dakshinamurti

St. Boniface Hospital

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Shyamala Dakshinamurti

Children's Hospital Research Institute of Manitoba

Kovvuri Jawahar Lal

University of Manitoba

Naranjan S. Dhalla

St. Boniface Hospital

Michael P. Czubryt

University of Manitoba

Sorin Musat

National Institute of Research and Development for Optoelectronics

Xi Wang

Chinese Academy of Medical Sciences & Peking Union Medical College

Anton Lukas

University of the Free State

Nobuakira Takeda

Jikei University School of Medicine

Jasbir Chauhan

University of Manitoba

Leonard S. Golfman

The University of Texas MD Anderson Cancer Center

Cooperative Institutions

University of Manitoba

St. Boniface Hospital

Children's Hospital Research Institute of Manitoba

Research Manitoba

University of Alberta

The Jikei University Hospital

Katsushika Medical Center

Harvard University

University of North Dakota

University of Arkansas for Medical Sciences

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Regulation of Calcium Influx Into Vascular Smooth Muscle by Vitamin B6

Clinical and Experimental Hypertension (1993)

Kovvuri Jawahar Lal Sushil Sharma Krishnamurti Dakshinamurti

In the vitamin B6 deficiency-induced hypertensive (B6DHT) rat there is an increased influx of calcium into the vascular smooth muscle. Vitamers which possess vitamin B6 activity blocked the in vitro calcium influx into the caudal artery of B6DHT rats and the BAY K 8644-induced influx into artery segments from vitamin B6-supplemented (control) rats. BAY K 8644 did not increase further the calcium influx into caudal artery segments from B6DHT rats. However, when this influx was partly decreased by Nifedipine or by pyridoxal phosphate, BAY K 8644 antagonized their effects indicating that calcium influx mediated by the dihydropyridine-sensitive calcium channel is a site of the calcium influx defect in the B6DHT rat.

10.3109/10641969309041624

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Citations (17)

Molecular and Cellular Biochemistry (1998)

Krishnamurti Dakshinamurti Kovvuri Jawahar Lal Pallab K. Ganguly

Calcium in biology

10.1023/a:1006832810292

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Citations (31)

Biotin

Vitamins and hormones (1989)

Krishnamurti Dakshinamurti Jasbir Chauhan

Biocytin

Biotin deficiency

Biotinidase deficiency

10.1016/s0083-6729(08)60398-2

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Citations (71)

Vitamin B6: Effects of Deficiency, and Metabolic and Therapeutic Functions

Springer eBooks (2017)

Krishnamurti Dakshinamurti Shyamala Dakshinamurti Michael P. Czubryt

Pyridoxamine

Pyridoxal phosphate

10.1007/978-3-319-40007-5_81-1

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Citations (8)

Effects of Biotin Deprivation and Biotin Supplementation

Springer eBooks (2019)

Krishnamurti Dakshinamurti Shyamala Dakshinamurti Michael P. Czubryt

Biotin deficiency

Biotinidase deficiency

10.1007/978-3-319-55387-0_73

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Citations (1)

Effects of Biotin Deprivation and Biotin Supplementation

Springer eBooks (2017)

Krishnamurti Dakshinamurti Shyamala Dakshinamurti Michael P. Czubryt

Biotin deficiency

10.1007/978-3-319-40007-5_73-1

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Binding proteins for α-tocopherol, L-ascorbic acid, thiamine amd vitamin B₆

Cambridge University Press eBooks (1994)

Krishnamurti Dakshinamurti Jasbir Chauhan

Vitamin E is the generic term for two groups of naturally occurring fat-soluble compounds, the tocopherols and the tocotrienols (Kasperek, 1980). In the tocopherols, the side chain is saturated; in the tocotrienols, it is unsaturated. The members of each group are designated α, β, γ, and δ depending on the number and position of methyl groups attached to the chroman nucleus. The most biologically active of these compounds is α-tocopherol, which inhibits the peroxidation of membrane lipids. This protection is dependent on the incorporation of α-tocopherol into membranes, and the extent of protection is related to the quantity of tocopherol present in membranes. Vitamin E is found primarily in intracellular membranes at concentrations of one to two orders of magnitude higher than that in the soluble fraction of various tissues (Taylor et al., 1976). In tissue homogenates, α-tocopherol is associated with amphiphilic and protein molecules and does not occur in the free form.

alpha-Tocopherol

10.1017/cbo9780511525391.009

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Nutrients and Cell Signaling

CRC Press eBooks (2005)

Janos Zempleni Krishnamurti Dakshinamurti

Cell signaling is at the core of most biological processes from the simplest to the most complex. In addition to unicellular organisms possessing the essential ability to receive inputs with regard to nutrient availability and noxious stimuli, the cells in multicellular organisms require signaling from adjacent, as well as distant cells to maintain

10.1201/9781420028362

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Microarray analysis of pancreatic gene expression during biotin repletion in biotin-deficient rats

Canadian Journal of Physiology and Pharmacology (2015)

Krishnamurti Dakshinamurti Rushita A. Bagchi Bernard Abrenica Michael P. Czubryt

Biotin is a B vitamin involved in multiple metabolic pathways. In humans, biotin deficiency is relatively rare but can cause dermatitis, alopecia, and perosis. Low biotin levels occur in individuals with type-2 diabetes, and supplementation with biotin plus chromium may improve blood sugar control. The acute effect on pancreatic gene expression of biotin repletion following chronic deficiency is unclear, therefore we induced biotin deficiency in adult male rats by feeding them a 20% raw egg white diet for 6 weeks. Animals were then randomized into 2 groups: one group received a single biotin supplement and returned to normal chow lacking egg white, while the second group remained on the depletion diet. After 1 week, pancreata were removed from biotin-deficient (BD) and biotin-repleted (BR) animals and RNA was isolated for microarray analysis. Biotin depletion altered gene expression in a manner indicative of inflammation, fibrosis, and defective pancreatic function. Conversely, biotin repletion activated numerous repair and anti-inflammatory pathways, reduced fibrotic gene expression, and induced multiple genes involved in pancreatic endocrine and exocrine function. A subset of the results was confirmed by quantitative real-time PCR analysis, as well as by treatment of pancreatic AR42J cells with biotin. The results indicate that biotin repletion, even after lengthy deficiency, results in the rapid induction of repair processes in the pancreas.

Biotin deficiency

10.1139/cjpp-2014-0517

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Citations (7)

Vitamins and their derivatives in the prevention and treatment of metabolic syndrome diseases

Endocrinology and Metabolic Syndrome (2013)

Krishnamurti Dakshinamurti

Omics

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