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Results for “clonality”

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PubMed1991

Diagnostic relevance of clonal cytogenetic aberrations in malignant soft-tissue tumors.

BACKGROUND: Malignant soft-tissue tumors often present substantial diagnostic challenges. Chromosome aberrations that might be diagnostic have been identified in some types of soft-tissue tumors, but the overall frequency and diagnostic relevance of these aberrations have not been established. METHODS: We attempted to determine the karyotypes of a series of 62 consecutive, unselected malignant spindle-cell or small round-cell soft-tissue tumors (from 46 adults and 16 children) after direct harvesting of cells or short-term culture. All tumors were examined independently by immunohistochemical staining in addition to routine light-microscopical evaluation, and all but two tumors were examined by electron microscopy. RESULTS: Metaphases were obtained from 61 of the 62 tumors, and clonal chromosome aberrations were identified in 55 (89 percent). In the six tumors that yielded metaphases but lacked apparent clonal aberrations, the normal metaphases were found to originate from non-neoplastic stromal elements within the tumor specimens. Thus, all tumors in which karyotyping was successful contained clonal chromosome aberrations. Forty of 62 tumors (65 percent) contained clonal chromosome aberrations that either suggested or confirmed a specific diagnosis; in 15 of these tumors (24 percent of all tumors), the aberrations were important in establishing the final diagnosis. Cytogenetic analyses were particularly informative about small round-cell tumors from children: 8 of 14 round-cell tumors contained diagnostically important chromosome aberrations. Using the combined approaches of light and electron microscopy, immunohistochemistry, and cytogenetics, we established an unambiguous diagnosis for 60 of 62 tumors. CONCLUSIONS: Cytogenetic analyses reveal clonal chromosome aberrations in virtually all malignant soft-tissue tumors. These clonal chromosome aberrations, particularly in small round-cell tumors in children, often have diagnostic relevance.

Adult↗

PubMed2001

DNA synthesis and mitotic clonal expansion is not a required step for 3T3-L1 preadipocyte differentiation into adipocytes.

Upon differentiation induction of 3T3-L1 preadipocytes by a hormone mixture containing 1-isobutyl-3-methylxanthine, dexamethasone, and insulin, the preadipocytes undergo approximately 2 rounds of mitotic clonal expansion, which just precedes the adipogenic gene expression program and has been thought to be an essential early step for differentiation initiation. By inducing 3T3-L1 preadipocytes with each individual hormone, it was determined that the mitotic clonal expansion was induced only by insulin and not by 1-isobutyl-3-methylxanthine or dexamethasone. Cell number counting and fluorescence-activated cell-sorting analysis indicated that a significant fraction of 3T3-L1 preadipocytes differentiated into adipocytes without mitotic clonal expansion when induced with the combination of 1-isobutyl-3-methylxanthine and dexamethasone. Furthermore, when normally induced 3T3-L1 preadipocytes were treated with PD98059 (an inhibitor of mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1) to block the activation of extracellular signal-regulated kinase (Erk) 1 and Erk2, the mitotic clonal expansion was blocked, but adipocyte differentiation was not affected. These observations were confirmed by bromodeoxyuridine labeling. The differentiated adipocytes induced with 1-isobutyl-3-methylxanthine and dexamethasone or standard hormone mixture plus PD98059 were not labeled by bromodeoxyuridine. Thus, it is evident that 3T3-L1 preadipocytes could differentiate into adipocytes without DNA synthesis and mitotic clonal expansion. Our results also suggested that activation of Erk1 and Erk2 is essential to but not sufficient for induction of mitotic clonal expansion.

1-Methyl-3-isobutylxanthine↗

PubMed2006

Molecular immunoglobulin/T-cell receptor clonality diagnosis by gene scan in lymphoproliferative disorders.

There remains significant controversy over the techniques used for clonal diagnosis of lymphoproliferative disorders because of questions regarding the sensitivity, specificity and throughput. This has stimulated us to explore the use of gene scan to determine clonality of Immunoglobulin (Ig)/T-cell receptor (TCR) (gamma gene rearrangement in a variety of morphologically, cytochemically, pathologically and immunophenotypically defined precursor B/T-ALL (12 patients), 5 patients with NHL, 10 patients with CLL and a group of reactive lymphocytosis as a reference group (10 subjects). Polymerase chain reaction (PCR) was done for IgH gene (FR3a, FR2b, LJH and JH primers) and for TCR gamma gene and the malignant clone was identified using gene scan (GS) analysis. In the ALL group, monoclonality was detected using GS and using IgH (FR2b) 75% had a clonal band, 63% with IgH (FR3a) and 88% with a combination of FR3a/FR2b. The results of TCR gamma monoclonality were 50% using primer mix I, 25% using primer mix II and 75% using a combination. In the CLL group, clonal IgH gene rearrangement was detected by FR2b in 80% of cases, while by FR3a clonal rearrangement was detected in 60%, the combination of FR2b and FR3a increased the detection rate to 90%. In B-cell NHL, the FR2b was clonally rearranged in 50% while FR3 was positive in 25%. In reactive lymphocytosis, all cases revealed polyclonal rearrangement with TCR gamma primers. The sensitivity and positive predictive value of GS was 100% and the specificity and negative predictive value was 86.6%. In conclusion, gene scanning provides a sensitive and specific method for detection of the malignant clone in PCR product in patients with lymphoproliferative disorders.

Electrophoresis, Capillary↗

PubMed2004

Clonal T-cell receptor gamma and delta gene rearrangements in T-cell acute lymphoblastic leukemia at diagnosis: predictor of prognosis and response to chemotherapy.

Risk-based treatment assignment requires the availability of prognostic factors that reliably predict clinical outcome. Junctional regions of T-cell receptor (TCR) genes provide the best tool to study clonality, lineage association and minimal residual disease (MRD) in T-ALL. In this study, we have analyzed the suitability of clonal TCR gamma and delta junctional gene rearrangement status of T-ALL patients at diagnosis as a prognostic marker for T-ALL. We studied peripheral blood samples of 50 newly diagnosed patients with T-ALL in India for incidence of clonal TCR gamma and delta junctional region gene rearrangements by PCR-coupled heteroduplex analysis. Of these, 17 T-ALL patients uniformly treated on MCP 841 protocol were followed for more than 40 months (range: 41.26-55.82 months; mean: 49.26) and their clonal TCRgammadelta genotype was correlated with clinical outcome with respect to duration of complete remission, disease-free survival (DFS) and event-free survival. We also compared the clinical and biological features of TCRgammadelta + T-ALL and TCRalphabeta + T-ALL for their relative order of significance. Thirty per cent (15 of 50) of Indian T-ALL patients exhibited clonal rearrangements of both TCR gamma and delta genes. A significant proportion of these patients (73.3%, 11 of 15 P < 0.005) showed predominant usage of VgammaI-Jgamma1.3/2.3 with Vdelta1-Jdelta1 genes. A statistically significant association of L2 and L1 FAB blast morphology with TCRgammadelta + T-ALL and TCRalphabeta + T-ALL, respectively was observed (P = 0.001 by Fisher's Exact Test). The survival rate in DFS group was higher for TCRgammadelta + T-ALL compared to TCRalphabeta + T-ALL (P = 0.1378 by Log rank test). Thus we have identified clonal TCR gamma and delta junctional gene rearrangement status of T-ALL patients at diagnosis as a prognostic marker and predictor of response to chemotherapy. In future, this may help in designing tailored and risk-adjusted (less aggressive and less toxic) therapies for subset of T-ALL patients.

Adolescent↗

PubMed2005

Virulence in mice of pneumococcal clonal types with known invasive disease potential in humans.

Streptococcus pneumoniae isolates of serotypes 1, 4, 6B, 7F, 14, and 19F belonging to clonal types with known invasive disease potential in humans were used to infect C57BL/6 and BALB/c mice. Most isolates were able to colonize the nasopharynx for 7 days. One serotype 19F isolate of the clonal type ST162 had higher bacterial numbers than other isolates and clonal types of the same serotype. Serotype 4 clones caused the most-severe invasive disease, whereas serotype 1 clones caused low-level bacteremia without disease symptoms. BALB/c mice were more likely than C57BL/6 mice to develop meningitis. Disease kinetics varied significantly between clonal types. Although most induced a robust tumor necrosis factor response, some isolates of serotype 1 and 7F did not, suggesting that invasive disease caused by different clonal types may result in different degrees of host response. Capsular serotype, other clonal properties, and host factors are important for the development of pneumococcal disease.

Animals↗

PubMed1994

Clonal analysis of posttransplant lymphoproliferative disorders, using both episomal Epstein-Barr virus and immunoglobulin genes as markers.

The authors analyzed the clonality of 15 samples of B-cell lymphoproliferations arising in eight organ allograft recipients, using immunoglobulin (Ig) gene rearrangement and the fused terminal fragment of episomal Epstein-Barr virus (EBV) DNA as independent clonal markers. The tumors arose from 1 month to 4 years following transplantation. All tumors were monomorphous, high-grade lymphomas of immunoblastic (6 cases), large-cell noncleaved (centroblastic, 1 case), or small noncleaved (1 case) type. All tumors were highly aggressive and failed to respond to decreased immunosuppression alone. Each tumor had clonal Ig gene rearrangements, including those that were negative for surface Ig. In 13 of 15 specimens (seven of the eight cases), the tumors also contained latent, circularized EBV genome. In 10 specimens from six patients, the tumors contained a single predominant form of episomal EBV DNA, indicating clonal cellular proliferation of an EBV-infected progenitor cell. Three specimens from one patient showed more than one band of episomal EBV DNA, suggesting oligoclonal expansion, despite the detection of only a single clone by Ig gene rearrangement. Linear replicating EBV DNA was not detected in any of the cases. Synchronous or metachronous specimens from multiple sites were studied in five patients, four of which were EBV-positive cases. Two patients had identical Ig gene arrangements in each specimen, indicating a single neoplastic clone at all sites; one case was EBV-negative, and the other had identical EBV episomes in each specimen. In the other three cases, apparently different Ig gene rearrangements were found at different sites. In two of these, however, the same predominant EBV episome was present at each site, indicating a common clonal origin. The third case had oligoclonal EBV bands in each specimen, with distinct patterns in at least two different sites, suggesting true multiclonality. Analysis of EBV genomes is a useful adjunct to Ig gene analysis in assessing the clonality of these lesions.

Adult↗

PubMed2002

Microsatellite analysis of primary and recurrent glial tumors suggests different modalities of clonal evolution of tumor cells.

Gliomas are characterized by highly variable biological behavior. After surgical resection and postoperative therapy they frequently recur with the same or higher-grade histology. Although a number of genetic aberrations have been described in gliomas of different histological types, the molecular mechanisms of the histological and clinical progression are poorly understood. In this study, we performed longitudinal microsatellite and mismatch repair gene analysis in paired samples of primary and recurrent gliomas in order to reveal whether genetic instability is associated with tumor progression. The 7 microsatellite loci of the 7 patients displayed a total of 18 (54.5%) alterations in the primary and 15 (45.5%) alterations in the recurrent gliomas as compared with the corresponding non-neoplastic cells, but no alterations were found in the hMLH1 and hMSH2 genes. These results suggest that microsatellite instability is associated with the development of the primary gliomas rather than with the recurrence or progression, and it is not associated with structural alterations in the hMLH1 or hMSH2 genes. Comparison of the microsatellite patterns in primary and secondary gliomas revealed 4 different modalities of clonal evolution, involving clonal identity, clonal deletion, clonal progression, and different clonality, suggesting that intensive clonal selection may play a central part in the recurrence of gliomas.

Adult↗

PubMed2001

Pulmonary Langerhans' cell histiocytosis: molecular analysis of clonality.

Pulmonary Langerhans' cell histiocytosis (LCH) is a form of Langerhans' cell disease that primarily affects smokers in the third to fifth decade. Extrapulmonary manifestations are rare. Its clinical course is typically characterized by stabilization or regression of bilateral micronodular infiltrates seen on chest radiographs; progression to honeycomb fibrosis is rare. Because the clinical course of pulmonary LCH is distinct from systemic multiorgan LCH, currently thought to be a clonal proliferative disorder, we examined the X-linked polymorphic human androgen receptor assay (HUMARA) locus to assess clonality in female patients with one or more discrete LCH cell nodules in open lung biopsies. Langerhans' cells (LCH cells) were excised from formalin-fixed, paraffin-embedded tissue by microdissection to assure a relatively pure cellular population, and studies for differential methylation patterns at the HUMARA locus were performed. Twenty-four nodules in 13 patients were evaluated. Seven (29%) were clonal and 17 (71%) were nonclonal. Of six cases with multiple discrete nodules, three (50%) showed a nonclonal LCH cell population. In one biopsy with five nodules, two nodules were clonal with one allele inactivated, one nodule was clonal with the other allele inactivated, and two nodules were nonclonal. In contrast to systemic LCH, pulmonary LCH appears to be primarily a reactive process in which nonlethal, nonmalignant clonal evolution of LCH cells may arise in the setting of nonclonal LCH cell hyperplasia. Cigarette smoking may be the stimulus for pulmonary LCH in contrast to other forms of LCH.

Adult↗

PubMed2000

Sensitive detection of clonal immunoglobulin rearrangements in frozen and paraffin embedded tissues by polymerase chain reaction heteroduplex analysis.

Molecular detection of a clonal population of B or T cells through analysis of rearranged antigen receptor genes is an essential adjunct to the morphologic, flow cytometric, and immunohistochemical evaluation of tissue specimens for the presence of leukemia or lymphoma. Combining polymerase chain reaction (PCR) with heteroduplex annealing and polyacrylamide gel electrophoresis (PAGE) has been used to detect clonal T-cell receptor rearrangements, particularly in skin biopsy specimens. The authors have developed a similar PCR heteroduplex assay for detection of clonal VDJ immunoglobulin gene rearrangements using two sets of primers based on relatively conserved consensus regions in the J(H) and framework I and 2 regions of the immunoglobulin heavy chain V region gene. This method is able to detect a clonal rearrangement when the clone comprises as little as 1% of the population in a polyclonal B-cell background. It may be used on fresh, frozen, or paraffin-embedded tissue and detects a clonal population in a majority of lymphoma subtypes. Compared with conventional PCR analysis, this method requires only a short additional cycle of denaturation and slow renaturation before PAGE. Interpretation is simplified as the clonal PCR product migrates away from the polyclonal background products.

Antibodies, Monoclonal↗

PubMed2001

PCR techniques for clonality assays.

Clonal overgrowths represent the hallmark of neoplastic proliferations, and their demonstration has been proved useful clinically for the diagnosis of malignant lymphomas based on the detection of specific and dominant immunoglobulin and/or T-cell receptor gene rearrangements. Nonrandom genetic alterations can also be used to test clonal expansions and the clonal evolution of neoplasms, especially analyzing hypervariable deoxyribonucleic acid (DNA) regions from patients heterozygous for a given marker. These tests rely basically on the demonstration of loss of heterozygosity (LOH) resulting from either hemizygosity (nonrandom interstitial DNA deletions) or homozygosity of mutant alleles observed in neoplasms. LOH analyses identify clonal expansions of a tumor cell population, and point to monoclonal proliferation when multiple and consistent LOH are demonstrated. Based on the methylation-related inactivation of one X chromosome in female subjects, X-linked markers (e.g., androgen receptor gene) will provide clonality information using LOH analyses after DNA digestion with methylation-sensitive restriction endonucleases. Therefore, both non-X-linked and X-linked analyses give complementary information, related and not related to the malignant transformation pathway respectively. Applied appropriately, these tools can establish the clonal evolution of tumor cell populations (tumor heterogeneity), identify early relapses, distinguish recurrent tumors from other metachronic neoplasms, and differentiate field transformation from metastatic tumor growths in synchronic and histologically identical neoplasms.

Clone Cells↗

PubMedDate not supplied

Childhood B lineage acute lymphoblastic leukemia clonality study by the polymerase chain reaction.

PURPOSE: B cell precursors acute lymphoblastic leukemia (ALL) present rearrangements in the heavy chain immunoglobulin and T cell receptor genes, especially in the complementarity determining region 3 (CDR-3) and T cell receptor delta (TCR delta) (V delta 2 D delta 3) regions. These rearrangements may be amplified by the polymerase chain reaction (PCR) and used as clonal markers of B lineage ALL. Our purpose was to study clonality at the DNA level by PCR in B lineage ALL. PATIENTS AND METHODS: Fifty-three pediatric patients (36 with B lineage ALL, 7 with ALL-T, and 10 with nonlymphocytic disease) were investigated using consensus primers for the CDR-3 regions of IgH and TCR delta. RESULTS: Clonality was detected in 86.1% of the patients with B lineage ALL when the primers for the CDR-3 regions were used, in 41.6% when the primers for TCR delta were used, and in 91.6% when the two primers were used together. Biclonality was found in 22.5% and 6.6% of patients that have shown clonality for CDR-3 and TCR delta, respectively. Clonality was not detected in any other samples using these primers. CONCLUSIONS: PCR using CDR-3 and TCR delta primers can be used as an aid for B lineage ALL diagnosis and clonal evolution of theses disease.

Burkitt Lymphoma↗

PubMed2003

Infection by the systemic fungus Epichloë glyceriae alters clonal growth of its grass host, Glyceria striata.

Parasites and pathogens are hypothesized to change host growth, reproduction and/or behaviour to increase their own transmission. However, studies which clearly demonstrate that parasites or pathogens are directly responsible for changes in hosts are lacking. We previously found that infection by the systemic fungus Epichloë glyceriae was associated with greater clonal growth by its host, Glyceria striata. Whether greater clonal growth resulted directly from pathogen infection or indirectly from increased likelihood of infection for host genotypes with greater clonal growth could not be determined because only naturally infected and uninfected plants were used. In this study, we decoupled infection and host genotype to evaluate the role of pathogen infection on host development and clonal growth. We found that total biomass production did not differ for clones of the same genotype, but infected clones allocated more biomass to clonal growth. Disinfected clones had more tillers and a greater proportion of their biomass in the mother ramet. Infected clones produced fewer tillers but significantly more and longer stolons than disinfected clones. These results support the hypothesis that pathogen infection directly alters host development. Parasite alteration of clonal growth patterns might be advantageous to the persistence and spread of host plants in some ecological conditions.

Adaptation, Physiological↗

PubMed1996

Clonality of basal cell carcinoma--molecular analysis of an interesting case.

Tumor cells represent a single clone of cells that have undergone a series of mutations in genomic DNA. This process, known as clonal evolution, is a distinguishing feature of cancer. The human androgen receptor gene (HUMARA; GenBank) contains a highly polymorphic cytosine-adenine-guanine trinucleotide repeat that can be used to determine clonality by depicting X chromosome inactivation patterns. Random X chromosome inactivation is consistent with polyclonality; nonrandom X chromosome inactivation indicates a clonal population of cells. Basal cell carcinoma (BCC) demonstrates an atypical growth pattern in that it grows slowly, rarely metastasizes, and is rarely lethal. Whether this tumor results from the accumulation of mutations in a single cell with subsequent clonal expansion or reflects a polyclonal response by a group of cells to a growth stimulus is unknown. To provide further insight into the molecular events characterizing BCCs, we determined the clonal origin of five modular BCCs from a female patient by analyzing X chromosome inactivation patterns at the HUMARA locus. All tumors demonstrated a nonrandom pattern of X chromosome inactivation, consistent with monoclonal proliferation. These findings provide strong genetic evidence that sporadic BCCs develop by clonal evolution and support the contention that a series of mutations in a single cell is responsible for the altered growth state seen in these transformed epithelial cells.

Aged↗

PubMed2000

Frequency and spatial patterning of clonal reproduction in Louisiana iris hybrid populations.

The plant genera in which natural hybridization is most prevalent tend to be outcrossing perennials with some mechanism for clonal (i.e., asexual) reproduction. Although clonal reproduction in fertile, sexually reproducing hybrid populations could have important evolutionary consequences, little attention has been paid to quantifying this parameter in such populations. In the present study, we examined the frequency and spatial patterning of clonal reproduction in two Louisiana iris hybrid populations. Allozyme analysis of both populations revealed relatively high levels of genotypic diversity. However, a considerable amount of clonality was apparent. Nearly half of all genets (47%) in one population and more than half (61%) in the other had multiple ramets. Furthermore, both populations exhibited relatively high levels of genetic structuring, a pattern that resulted from the aggregation of clonal ramets. The occurrence of clonal reproduction in hybrid populations could not only facilitate introgression through an increase in the number of flowering ramets per genet and/or the survivorship of early generation hybrids, but might also influence the mating system of such populations. Any potential increase in the selfing rate due to cross-pollination among ramets of the same genet may, in turn, increase the likelihood of homoploid hybrid speciation.

Biological Evolution↗

PubMed2004

Spatial genetic structure within a metallicolous population of Arabidopsis halleri, a clonal, self-incompatible and heavy-metal-tolerant species.

Arabidopsis halleri, a close wild relative of A. thaliana, is a clonal, insect-pollinated herb tolerant to heavy metals (Zn, Pd, Cd) and a hyperaccumulator of Zn and Cd. It is of particular interest in the study of evolutionary processes and phytoremediation. However, little is known about its population gene flow patterns and the structure of its genetic diversity. We used five microsatellite loci to investigate the genetic structure at a fine spatial scale (10 cm to 500 m) in a metallicolous population of A. halleri. We also studied the contributions made by clonal propagation and sexual reproduction (seed and pollen dispersal) to the genetic patterns. Clonal diversity was high (D(G) > 0.9). Clonal spread occurs only at short distances (< 1 m). Both clonal spread and limited dispersal, associated with sexual reproduction, contribute to the significant spatial genetic structure revealed by spatial autocorrelation analysis. The shape of the autocorrelogram suggests that seed dispersal is restricted and pollen flow extensive, which may be related to intense activity by insect pollinators. Clonal spread was more extensive in the lowly polluted zone than in the highly polluted zone. This cannot be interpreted as a strategy for promoting the propagation of adapted genotypes under the harshest ecological constraints (highest heavy metal concentrations). The higher fine-scale spatial genetic structure found in the lowly polluted zone can be ascribed to plant densities that were lower than in the highly polluted zone. No evidence of genetic divergence due to spatial heavy metal heterogeneity was found between lowly and highly polluted zones.

Analysis of Variance↗

PubMed2005

Maintenance of clonal diversity during a spring bloom of the centric diatom Ditylum brightwellii.

Maintenance of genetic diversity in eukaryotic microbes reflects a synergism between reproductive mode (asexual vs. sexual) and environmental conditions. We determined clonal diversity in field samples of the planktonic marine diatom, Ditylum brightwellii, during a bloom, when cell number increased by seven-fold because of rapid asexual division. The genotypes at three microsatellite loci were determined for 607 individual cell lines isolated during the 11 days of sampling. Genetic diversity remained high during the bloom and 87% of the cells sampled each day were genetically distinct. Sixty-nine clonal lineages were sampled two or more times during the bloom, and two clones were sampled seven times. Based on the frequency of resampled clonal lineages, capture-recapture statistics were used to determine that at least 2400 genetically distinct clonal lineages comprised the bloom population. No significant differences in microsatellite allele frequencies were observed among daily samples indicating that the bloom was comprised of a single population. No sexual stages were observed, although linkage equilibrium at two loci, high levels of allelic and genotypic diversity, and heterozygote deficiencies were all indicative of past sexual reproduction events. At the height of the bloom, a windstorm diluted cell numbers by 51% and coincided with a change in the frequency distribution of some resampled lineages. The extensive clonal diversity generated through past sexual reproduction events coupled with frequent environmental changes appear to prevent individual clonal lineages from becoming numerically dominant, maintaining genetic diversity and the adaptive potential of the population.

Diatoms↗

PubMed1992

Oligoclonal T cells in rheumatoid arthritis: identification strategy and molecular characterization of a clonal T-cell receptor.

Immunodominant antigens in rheumatoid arthritis (RA) should induce an expansion of T cells bearing a corresponding T-cell receptor (TCR). We therefore analysed the TCR repertoire at the site of inflammation using two fundamentally different strategies. The total TCR repertoire was examined by generating 'representative' T-cell clone panels, which were subsequently tested for clonality by restriction mapping of the TCR beta gene locus. No clonality was detected in large T-cell clone panels generated with cells from three patients. However, when we selectively analysed the TCR repertoire of in vivo pre-activated, interleukin-2 (IL-2)-responsive T cells, significant T-cell/TCR clonality was found in 2 out of 4 patients. The clonal T cells represented a minority of the total T-cell population with an estimated frequency of 1 in 300 to 1 in 1000 cells. Molecular characterization of a clonal TCR and the use of a specific TCR V beta MoAb ruled out an over-representation of T cells bearing the same V beta element in the total T-cell population, rendering the involvement of super-antigens in the induction of T-cell clonality in this case unlikely.

Amino Acid Sequence↗

PubMed1997

Supplemental melatonin increases clonal lifespan in the protozoan Paramecium tetraurelia.

The hypothesis that melatonin supplementation can increase the lifespan of a single-celled organism was tested by the administration of melatonin to the ciliated protozoan Paramecium tetraurelia. Melatonin supplementation in dim red light at a dose of 0.043 mM (10 mg/L) of nutrient media (bacterized Cerophyl) per day, followed by incubation for 23 hr in darkness, increased the mean clonal lifespan of Paramecium tetraurelia in days by percentages ranging from 20.8% (P < 0.01, two-tailed t-test) to 24.2% (P < 0.01, ANOVA) over controls. Maximum clonal lifespan in days was also increased in melatonin-supplemented cells, from 14.8% to 24.0% over controls. Mean clonal lifespan in fissions was not significantly greater in melatonin-supplemented cells, with values ranging from 6.0% to 15.5% over controls. Maximum clonal lifespan in fissions did not differ appreciably, with values ranging from 1.0% to 9.1% over controls, except in the case of cells selected for rapid division rates, in which melatonin-supplemented cells (393 fissions) lived 20.9% longer than controls (325 fissions) in terms of cumulative cell doublings during the clonal lifespan. The finding that melatonin supplementation increased clonal lifespan in Paramecium tetraurelia, an aerobic, single-celled organism, suggests that the mechanism of melatonin's longevity-promoting effects may be intracellular.

Animals↗