Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.1.21 (thymidine kinase)
 7,561 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin A (VA) protects the small intestine from the methotrexate (MTX)-induced damage. The in vivo effects of MTX and/or VA on crypt cells of small intestine were investigated using rats orally administered MTX (15 mg/kg body weight) and/or VA (5,000 IU/kg body weight). The thymidine kinase activity of crypt cells separated from villus cells of small intestine of MTX plus VA-treated rats was lower than that from control rats but higher than that from MTX-treated rats. VA-treated rats showed almost the same activity of thymidine kinase as control rats. The amounts of the end products, adenosine monophosphate (AMP) and guanosine monophosphate (GMP), contained in crypt cells of treated rats were determined to investigate the in vivo effects of MTX and/or VA on de novo purine synthesis. MTX treatment significantly decreased the amounts of both AMP and GMP but both amounts were not affected by MTX plus VA treatment. Treatment with VA alone appeared to increase their amounts slightly. Thus, although the oral administration of MTX to rats inhibited DNA synthesis in crypt cells, VA coadministration protected the salvage pathway of pyrimidine synthesis and the de novo purine synthesis in crypt cells.
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PMID:Protective effect of vitamin A against the methotrexate-induced damage to small intestine: a study on the crypt cells. 195 82

This study investigated the effect of clinical and subclinical vitamin A deficiency on intestinal structure and function in rats. Weanling male rats fed a vitamin A-deficient diet (VA-) for 40-42 or 60-63 d were compared with rats either pair-fed (PF) or with free access to the same diet supplemented with vitamin A (VA+). A reference (REF) group was fed a standard rat diet. Weight began to plateau in VA- rats after 42 d, becoming significantly different from PF rats at 60-63 d (P < 0.02). Diarrhea did not develop in any study group. VA- rats had clinical signs of vitamin A deficiency in the 60-63 d study, but not in the 40-42 d study. However, serum and liver retinol concentrations were negligible in all VA- rats. VA- rats in the 60-63 d study had significantly reduced villus height (P < 0.02), and sucrase and maltase activities (P < 0.02) compared with PF rats. There were no differences between VA- and PF rats in mucosal wet weights, protein and DNA concentrations, thymidine kinase activity and glucose transport. No differences were detected in the 40-42 d study for any variable measured. Because clinical vitamin A deficiency in rats causes only mild changes in intestinal structure and function, it is unlikely that these alterations alone are responsible for the interactions observed in epidemiological studies between vitamin A deficiency and diarrheal disease.
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PMID:Vitamin A-deficient rats have only mild changes in jejunal structure and function. 868 43

The composition and response of the retinoid signaling pathway in a human cell line (CC-1), representative of a low grade cervical carcinoma, were evaluated. Reverse-transcriptase polymerase chain reaction (RT-PCR) analysis demonstrated expression of cytoplasmic retinol binding protein, CRBPI, cytoplasmic retinoic acid binding protein, CRABPII, and nuclear retinoic acid receptors, RAR alpha, RARgamma, RXR alpha, and RXRbeta, but not CRABPI or RARbeta. This pattern is similar to that of the ectocervix. Activation of endogenous nuclear receptors was evaluated in a reporter subline of CC-1, called CC-B, containing a reporter gene controlled by a retinoic acid responsive element (RARE) and thymidine kinase promoter. Retinoid treatment of CC-B resulted in dose-dependent increases in reporter gene expression. Retinoids inhibited growth at concentrations greater than 100 nM. 9-cis retinoic acid (1 nM) significantly stimulated growth. Immunohistochemical analysis of CC-B organotypic cultures demonstrated a high level of epidermal growth factor receptor (EGF-R) expression that was decreased by retinoids. The degree of RARE transactivation induced by retinoids significantly correlated with the degree of inhibition of growth (R = -0.96) and EGF-R expression (R = -0.92). The dose-dependent and retinoid-specific responses of CC-1 at the molecular and biological levels demonstrate the utility of this reporter cell line for evaluation of retinoid activities.
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PMID:Biological assay for activity and molecular mechanism of retinoids in cervical tumor cells. 923 31