Planned parenthood and artifical selection.
Explore the source record for details and available documents.
Embryonic Development↗
Biomedical subjects
R Bamezai
Publications and source records attributed to R Bamezai.
Postnatal effect of arecoline on chlorophyllin-modulated hepatic biotransformation system enzymes in suckling neonate and lactating mice.
The present study evaluates the potential of arecoline alkaloid on chlorophyllin (CHL) modulated levels of hepatic biotransformation system enzymes in suckling neonate and lactating mice. CHL [50, 100, or 200 mg/kg body weight (b.w.)/day] induced significant increases in the hepatic levels of glutathione S-transferase (GST) and sulfhydryl (-SH) in lactating dams and suckling pups of 14 or 21 days. The depleted level of hepatic Cytochrome (Cyt.) P-450 was observed only in lactating dams given 200 mg/kg b.w. CHL. Arecoline (20 mg/kg b.w.) could depress the CHL-induced levels of hepatic GST and -SH, while Cyt. P-450 and Cyt. b5 levels remained unaltered by arecoline alone or arecoline plus CHL treatment. In lactating dams the modulated levels of hepatic biotransformation system enzymes potentially could affect the detoxication efficacy of administered chemicals besides influencing the rate and extent of passage of metabolites to suckling neonate.
Animals↗
Effect of arecoline on the curcumin-modulated hepatic biotransformation system enzymes in lactating mice and translactationally exposed F1 pups.
The present study assesses the potential of arecoline alkaloid to translactationally modify the chemopreventive efficacy of curcumin (diferuloyl methane) via neonatal modulation of hepatic biotransformation system enzymes. Curcumin (0.4 g/kg body wt/day) induced a significant increase in the hepatic levels of glutathione-S-transferase (GST), acid-soluble sulfhydryl (SH), cytochrome b5, and cytochrome P-450 in lactating dams and F1 pups at 14 or 21 days. Arecoline (20 mg/kg body wt/day) could not modulate the hepatic GST and SH levels, although significant induction was observed in the levels of cytochrome b5 and cytochrome P-450 in dams and suckling pups. Significant enhancement of hepatic GST, SH, cytochrome b5, and cytochrome P-450 levels was observed in groups treated with curcumin+arecoline. Curcumin-induced levels of GST and SH were depressed whereas cytochrome b5 and cytochrome P-450 were further elevated by curcumin+arecoline treatment. The elevated levels of Phase I enzymes were more significant with exposure to curcumin+arecoline than with arecoline exposure alone. Modulation in competing potential pathways of biotransformation system enzymes in lactating dams may affect the rate and extent of maternal detoxication and thus influence the passage of metabolites of administered xenobiotics to the suckling neonate.
Animals↗
Modulatory influence of chlorophyllin on the mouse skin papillomagenesis and xenobiotic detoxication system.
The present study evaluates the modulatory potential of chlorophyllin (CHL) on the murine skin papillomagenesis pattern and its influence on the levels of biotransformation system enzymes. Topical application of CHL (100 mg/kg body weight/day) during peri-, post- or peri- and post-initiational stages of 7,12-dimethylbenz[a]anthracene (DMBA)-induced papillomagenesis, significantly (P < 0.01) reduced the (i) tumor burden to 3.68, 3.56 and 3.33 (positive control value: 5.89); (ii) cumulative number of papillomas to 59, 57 and 60 (positive control value: 112); and (iii) incidence of mice bearing papillomas to 88%, 88% and 90%, respectively (positive control value 100%). CHL treatment alone or during peri-, post-, or peri- and post-initiational stages significantly elevated the glutathione S-transferase (GST) and -SH levels in the liver and skin tissue of the murine system. The potential of CHL in modulating the process of carcinogenesis is suggested by the altered levels of biotransformation system enzymes. The implications of the biochemical changes and inhibition of tumor incidence by CHL are discussed.
9,10-Dimethyl-1,2-benzanthracene↗
Bloom syndrome: is the gene mapped to the point?
Bloom syndrome (BS), an autosomal recessive genetic disorder, is an instructive model to explore variety of questions in "deregulation of normal cell functioning". Most of the BS patients are homozygous for mutant BLM gene and depict high sister chromatid exchanges (SCEs) in almost all the cells. However, a few possess cells with dimorphic SCE phenotype. A majority of patients with dimorphic SCE phenotype have been suggested to be compound heterozygotes, inheriting two different mutations in the BLM locus from each parent. An intragenic somatic recombination event in a precursor stem cell in such patients is envisaged to give rise to a population of cells with functionally wild-type (BLM) gene and normal SCE phenotype. Adopting unique dual approaches of positional mapping through "homozygosity by descent" and "somatic crossover point mapping", a candidate for BLM has been identified and localized to a 250 Kb interval between polymorphic loci, DI5S1108 and D15127. The sequence has been found to encode a 1417 amino acid peptide with homology to the RecQ helicases, a sub-family of DExH box-containing DNA and RNA helicases. The presence of chain terminating mutations in the 'candidate' gene in BS patients has suggested it to be the BLM gene. Apparantly the proposed gene product does not seem to provide answer for a variety of clinical, biochemical and experimental observations made in BS or BS cells till date. Our recent observation of a significant decrease in the activity of pyruvate kinase in three BS B-lymphoblastoid cell lines when compared to a similar cell line established from a normal healthy subject presents with another possible candidate to elucidate the defects in BS. Experiments using okadaic acid, a phosphatase-2a/1 inhibitor, have depicted in our study that many of the clinical features characteristic of BS, not easily explanable by the recently proposed BLM gene, can be explained by the deficiency in the PK alone and/or PP2a/PP1 activity.
Bloom Syndrome↗
Postnatal modulation of hepatic biotransformation system enzymes via translactational exposure of F1 mouse pups to turmeric and curcumin.
The potential for the transfer of active principle(s) of turmeric (Curcuma longa L.) and curcumin (major pigment in turmeric) via translactational route and its modulatory influence on the hepatic biotransformation system enzymes in the lactating dams and their suckling offspring was assessed. Turmeric (4 g/kg b.w. per day) and curcumin (0.4 g/kg b.w. per day) induced significant (P < 0.01) increase in the hepatic levels of glutathione S-transferase (GST) and acid soluble sulfhydryl (-SH) after 14 or 21 days treatment in lactating dams and translactationally exposed F1 pups. However the lower dose of curcumin (0.2 g/kg b.w. per day) could modulate hepatic GST activity (P < 0.05) and -SH (P < 0.01) only after 21 days of treatment in dams and pups. Cytochrome b5 and cytochrome P450 levels were significantly elevated (P < 0.05) in the dams as well as their suckling pups of both 14 and 21 days age groups at the selected dose levels of turmeric (4 g/kg b.w.) and curcumin (0.4 g/kg b.w.). The induction in hepatic biotransformation system enzymes in lactating dams and F1 progeny suggests the passage of active constituents and/or metabolites of turmeric and curcumin via the translactational route.
Animals↗
Induction of high SCEs in normal cells by 11-12 kDa plasma protein overexpressed in some sleep deprived volunteers.
The present study confirmed our earlier preliminary observation of induction of high SCEs in 1 day sleep-deprived healthy volunteers and showed that the property of induction of high SCE by after-sleep-deprived (ASD) plasma was retained both in 50% ammonium sulphate precipitates and in the dialysed plasma using a membrane of 12 kDa porocity. Further, nitrocellulose bound 11-12 kDa electrophoretically isolated plasma protein from ASD individuals was found responsible for the induction of high SCE in normal whole blood cultures. A short exposure of 3 h to 5% ASD plasma was enough to induce significantly high SCEs in normal lymphocytes which had undergone 2 replication cycles after the exposure to this factor.
Adult↗
Noise-free chemiluminescent detection of human T cell receptor and interleukin-2 receptor genes after optimization of digoxigenin labeled probe concentration.
Reduction in the background problems to improve the efficiency of nonradioactive labeling and detection procedure has been the focus of attention in the recent past for wider acceptance of the technique in nucleic acid research. We have achieved success in obtaining a relatively background free detection of single copy genes such as, T-cell receptor-delta (TCR-delta) and interleukin-2 receptor (L-2r) in human genome by using optimized concentrations of the digoxigenin labeled probes. Inclusion of such an optimization step for each probe before carrying out the actual hybridization experiment did not require any further modification in hybridization conditions and detection protocols as suggested earlier [Anal Biochem, 210 (1993) 235; Colloq Boehringer Mannheim, 2 (1991) 4.]
Blotting, Southern↗
Protein phosphatase-1 inhibition induces high SCEs in normal whole blood cultures.
Effect of 1,25,50 and 75 nM of okadaic acid (OA) on human lymphocytes from healthy individuals in culture has been investigated. To our surprise, we observed induction of significantly high sister chromatid exchanges (SCEs) at concentrations known to inhibit both protein phosphatase-1 (PP-1) and protein phosphatase -2A (PP-2A). However, 1 nM okadaic acid, known to inhibit PP-2A alone, did not induce this cellular feature/phenotype. This novel preliminary observation lays foundation for investigating further the role of PP-1 inhibition in governing as yet unknown finer controls in the induction of high SCEs, the mechanism for which has eluded answers till date.
Cells, Cultured↗
Sister chromatid exchange frequency in breast cancer cases.
Sister chromatid exchange (SCE) were studied in 22 patients with breast cancer (i.e., four stage II; 12 stage III, six stage IV) and 10 normal healthy females as age-matched controls. The data obtained in these cases followed a Poisson distribution. An apparent increase in the average rate of SCE/cell was observed with the advancing stage of breast cancer.
Breast Neoplasms↗
Sleep deprivation in human males and its effect on SCE rates in chromosomes--a preliminary study.
The present preliminary study on 5 healthy volunteers deprived of sleep for a day showed a considerable increase in sister-chromatid exchange (SCE) rate in the chromosomes after sleep deprivation. Although the rate of increase varied between the studied subjects, interestingly the 5% plasma from a volunteer with a statistically significant increase after sleep deprivation, when supplemented to cell cultures from an age-matched normal subject, induced high SCEs. This suggests the presence/absence of some factor(s) in plasma samples of subjects showing high SCEs after sleep deprivation, playing a role in the induction of high SCEs in normal cells exposed to the samples in vitro. The present study also suggests that there could be categories which may or may not respond to sleep deprivation with high SCE induction and their plasma supplemented to normal cell culture in turn may or may not induce high SCEs. Nevertheless, the pathophysiological role of high SCEs induced by sleep deprivation in some cases remains intriguing and unresolved and needs further extensive study.
Adult↗
Different mutations responsible for the elevated sister-chromatid exchange frequencies in Bloom syndrome and X-irradiated B-lymphoblastoid cell lines originating from acute leukemia.
Cell hybridization and co-cultivation protocols have been used to determine whether the increased rates of sister-chromatid exchanges (SCEs) exhibited by Bloom syndrome (BS) and a human mutant cell line (CCRF-SB-T1), originating from an X-irradiated acute leukemia-derived B-lymphoblastoid cell line, have the same or different bases. Cell fusion of CCRF-SB-T1 with each of 4 different BS B-lymphoblastoid cell lines (LCLs), retaining a high-SCE character, exhibited low (normal level) numbers of SCEs, signifying complementation. Co-cultivation of CCRF-SB-T1 and BS B-LCLs also resulted in a significant reduction in SCE level, from 70 to 35, in BS cells, lowered the BrdU concentrations necessary for sister-chromatid differential staining (SCD) from 15 micrograms/ml (0.05 mM) to 2.0 micrograms/ml (0.01 mM) and resulted in a completely normal level of SCE in CCRF-SB-T1 cells. This strongly suggests that the defects in the 2 cell types are different. In the assay of cell extracts, the 4 BS cell lines appear to have lost thymidylate (TMP) synthetase activity (about 50% reduction from that of normal cells), whereas CCRF-SB-T1 cells show a 20% increase of TMP synthetase activity compared to normal cells.
B-Lymphocytes↗
Differential BrdU uptake in 3 cell cycles and the resultant 3-way sister-chromatid differentiation at M3 endoreduplicated chromosome level--a hypothesis.
The M3 endoreduplicated chromosomes account for SCE1-3 in a compact form after 3-way sister-chromatid differentiation (3-way SCD). However, a difficulty is faced in the analysis and interpretation of these results. Keeping this in view, the present work attempts to explain a number of possibilities correlating the SCD patterns to the probable patterns of uptake of bromodeoxyuridine (BrdU) over 3 successive cell cycles in M3 endoreduplicated chromosomes. This has been done to facilitate understanding of the staining patterns which could be obtained in the M3 endoreduplicated chromosomes after 3-way SCD, and further for the speedy analysis of such chromosomes, especially in scoring SCE1-3 precisely.
Bromodeoxyuridine↗
Frequency of acrocentric association in abnormal sexual development in males and females.
A significant difference (P less than 0.05) was observed in a chi 2 comparison of DD, GG and DG-DI associations between male hypogonads and females with primary amenorrhea. This difference increased still further (P less than 0.01) when only DD and GG associations were compared between males and females with abnormal sexual development (ASD). Similarly, when normal males and females were compared for DI, TRI, TETRA, DD vs GG and DG vs GG acrocentric chromosome associations, a significant difference (P less than 0.05) was again observed. The sex difference was also apparent in TRI and TETRA acrocentric associations both in abnormal and normal sexual development males and females. These results suggested that probably sex difference (may be hormonal) influences the number and/or type of acrocentric chromosomes involved in association between males and females with ASD and also between normal males and females.
Amenorrhea↗
Chromatid association in acrocentric chromosomes of abnormal sexual development (ASD) cases.
Concordant/discordant associations at chromatid level were compared and found significant (P less than 0.05) in females with primary amenorrhea. This probably suggested that the acrocentric association pattern in this group of ASD and infertility did not follow a random segregation in subsequent cell divisions and that the concordant acrocentric chromosomes have regularly established physical connections with one another, held together for several cell cycles. It could only be speculated that the association of acrocentric chromosome anomalies in some females with abnormal sex chromosomes are due to this reason. In the event that chromosome association has a bearing on chromosome aberrations, the non-random pattern of acrocentric association probably would increase the choice for translocation and non disjunction in the somatic cells in females with primary amenorrhea during ontogenesis.
Amenorrhea↗
Sister-chromatid exchange (SCE) rate in normal and abnormal sexual development in males and females.
Thirty-three patients with abnormal sexual development (9 male hypogonads, 20 females with primary amenorrhea and 4 cases of ambiguous genitalia), 10 normal males and 8 normal females (below the age of 30 years) were evaluated for SCE/cell and for SCE distribution according to chromosome groups (A to G). Smokers and alcoholics and subjects under medication were excluded from the study. The average rates of SCE/cell in male hypogonads, primary amenorrhea and ambiguous genitalia were 4.23 +/- 1.51, 4.02 +/- 0.90 and 4.33 +/- 1.34, respectively, whereas in normal males and females the average rates were 4.27 +/- 0.69 and 4.49 +/- 0.87, respectively. The SCE data followed a Poisson distribution. Chi-square testing showed a statistically significant difference only in B-group chromosomes when male hypogonads were compared with normal males (p less than 0.02) and females with primary amenorrhea were compared with normal females (p less than 0.02), suggesting the importance of the study of SCE frequency distribution at chromosome group level to bring out the differences otherwise concealed in average rates.
Adult↗
Visualization and comparison of protein bands in the same SDS-PAG with simultaneous use of three different stains.
Explore the source record for details and available documents.
Animals↗
Folate sensitive and BrdU dependent fragile sites on human chromosomes.
Explore the source record for details and available documents.
Bromodeoxyuridine↗