Effects of ginger (Zingiber officinale Roscoe) on DNA damage and development of urothelial tumors in a mouse bladder carcinogenesis model

Extracts of the spice ginger (Zingiber officinale Roscoe) are rich in gingerols and shogaols, which exhibit antioxidant, anti-inflammatory, antifungal, anti mycobacterial, and anticarcinogenic proprieties. The present study evaluated the chemoprotective effects of a ginger extract on the DNA damage and the development of bladder cancer induced by N-butyl-N-(4-hydroxibutyl) nitrosamine (BBN)/N-methyl-N-nitrosourea (MNU) in male Swiss mice. Groups G1-G3 were given 0.05% BBN in drinking water for 18 weeks and four i.p. injections of 30 mg/kg body weight MNU at 1, 3, 10, and 18 weeks. Group G4 and G5 received only the BBN or MNU treatments, respectively, and groups G6 and G7 were not treated with BBN or MNU. Additionally, Groups G2, G3, and G6 were fed diets containing 1, 2, and 2% ginger extract, respectively, while Groups G1, G4, G5, and G7 were fed basal diet. Samples of peripheral blood were collected during the experiment for genotoxicity analysis; blood collected 4 hr after each MNU dose was used for the analysis of DNA damage with the Comet assay (assay performed on leukocytes from all groups), while reficulocytes collected 24 hr after the last MNU treatment of Groups G5-G7 were used for the micronucleus assay. At the end of the experiment, the urinary bladder was removed, fixed, and prepared for histopathological, cell proliferation, and apoptosis evaluations. Ginger by itself was not genotoxic, and it did not alter the DNA damage levels induced by the BBN/MNU treatment during the course of the exposure. The incidence and multiplicity of simple and nodular hyperplasia and transitional cell carcinoma (TCC) were increased by the BBN/MNU treatment, but dietary ginger had no significant effect on these responses. However, in Group G2 (BBN/MNU/2% ginger-treated group), there was an increased incidence of Grade 2 TCC. The results suggest that ginger extract does not inhibit the development of BBN-induced mouse bladder tumors.

Cytodifferentiation during the spermatogenesis of the hermaphrodite caridea Exhippolysmata oplophoroides

Among the decapods, the caridean Exhippolysmata oplophoroides has been described as a simultaneous protandric hermaphrodite, seeing that it presents a male initial stage followed by a hermaphrodite one in which it can function as male and as female. This work had the aims of characterizing the microscopical morphology of the male portion of the ovotestes gonads from E. oplophoroides, at the different development stages, identifying each cell from the germ lines during spermatogenesis, as well as describing the ultramorphology of spermatozoans in the terminal region of the vasa deferentia. Shrimps were collected in Ubatuba, north coast of São Paulo, and their male gonads and the ampoule were removed, fixed and processed according to histological routine and for scanning electron microscopy. The testicular portion is divided in lobes, inside which cells at the same stage of the spermatogenic cycle are observed, with prevalence of spermatogonia and spermatocytes at stages I, II and V of gonad development, whereas spermatids and spermatozoans are found at stages III and IV, respectively. Ultramorphology of the terminal portion of the vasa deferentia exhibits mature aflagellated spike-shaped spermatozoans, encased in secretion and between membrane foldings that will constitute the spermatophores. Despite presenting reproductive characteristics common to other decapods. E. oplophoroides shows spermatozoans as well as spermatophore with typical morphology, which is important for its identification and taxonomy. Further, this species showed polysaccharide secretions where the spermatozoa are immerse as far as the testicular portion, which could have a roe in their transport and nutrition as well as spermatophore constitution and/or fixation; differently, other caridean species begin spermatophore formation during the passage of the gametes through the vasa deferentia. (C) 2010 Elsevier Ltd. All rights reserved.

Ultrastructural analysis of the effect of mating delay on cell death in the ovaries of virgin honey bee (Apis mellifera L.) queens

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Gene expression profiling reveals molecular marker candidates of laryngeal squamous cell carcinoma

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Genomic imbalances in esophageal squamous cell carcinoma identified by molecular cytogenetic techniques

This review summarizes the chromosomal changes detected by molecular cytogenetic approaches in esophageal squamous cell carcinoma (ESCC), the ninth most common malignancy in the world. Whole genome analyses of ESCC cell lines and tumors indicated that the most frequent genomic gains occurred at 1, 2q, 3q, 5p, 6p, 7, 8q, 9q, 11q, 12p, 14q, 15q, 16, 17, 18p, 19q, 20q, 22q and X, with focal amplifications at 1q32, 2p16-22, 3q25-28, 5p13-15.3, 7p12-22, 7q21-22, 8q23-24.2, 9q34, 10q21, 11p11.2, 11q13, 13q32, 14q13-14, 14q21, 14q31-32, 15q22-26, 17p11.2, 18p11.2-11.3 and 20p11.2. Recurrent losses involved 3p, 4, 5q, 6q, 7q, 8p, 9, 10p, 12p, 13, 14p, 15p, 18, 19p, 20, 22, Xp and Y. Gains at 5p and 7q, and deletions at 4p, 9p, and 11q were significant prognostic factors for patients with ESCC. Gains at 6p and 20p, and losses at 10p and 10q were the most significant imbalances, both in primary carcinoma and in metastases, which suggested that these regions may harbor oncogenes and tumor suppressor genes. Gains at 12p and losses at 3p may be associated with poor relapse-free survival. The clinical applicability of these changes as markers for the diagnosis and prognosis of ESCC, or as molecular targets for personalized therapy should be evaluated.

Epigenetic Silencing of CRABP2 and MX1 in Head and Neck Tumors

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Differentially expressed genes in giant cell tumor of bone

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Effects of myenteric denervation on extracellular matrix fibers and mast cell distribution in normal stomach and gastric lesions

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Immunohistochemical study of the expression of fatty acid synthase and Ki-67 in salivary gland tumors

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Pigmentação testicular em Physalaemus nattereri (Steindachner) (Amphibia, Anura) com observações anatômicas sobre o sistema pigmentar extracutâneo

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Long term evaluation of morphometric and ultrastructural changes of testes of alloxan-induced diabetic rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Emprego do cell block de agarose como método complementar no diagnóstico citológico de tumores mamários caninos

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Radioprotection of beta-carotene evaluated on mouse somatic and germ cells

In the present paper, the protective effect of beta-carotene was evaluated after whole body exposure of mice to 2 Gy of X-rays. Splenocytes, reticulocytes, bone marrow cells and spermatids were evaluated for the frequency of micronuclei (MN) induced by X-rays. Mice were treated (gavage) with beta-carotene (10, 25 and 50 mg/kg b.w.) for 5 consecutive days and, 4 h after the last treatment, the animals were irradiated. The results obtained showed different frequencies of X-ray-induced-MN between different cell populations analysed and also different response of these cells to the beta-carotene treatment. The radioprotective effect of beta-carotene was observed in splenocytes, reticulocytes, and spermatids but not in bone marrow cells. No dose-response relationship for beta-carotene was detected. The time of sampling, the sensitivity of the cells as well as the antioxidant activity of beta-carotene are discussed as important factors for the radioprotective action of this provitamin.

DETECTION OF CELL-PROLIFERATION IN TISSUE-SECTIONS

1. Cell proliferation is of interest since abnormal cell proliferation appears to be a precursor of tumorigenesis and also because the quantitative description of cell proliferation in tumors can be used to predict the biological behavior of a particular neoplasia.2. Them am several reliable methods of studying cell proliferation in tissues. One of the most important is the detection of the Ki67 defined antigen in frozen sections. The number of cells expressing Ki67 correlates with histological grades of tumors and can also be predictive of clinical outcome. The Ki67 can be localized in tissue sections using monoclonal antibodies in association with the immunoperoxidase technique.3. Proliferating cell nuclear antigen (PCNA) is a component of DNA polymerase-delta and is another important cell proliferation marker manifesting a striking increase in concentration during the S phase of the cell cycle. 19A2 and PC10 are two different monoclonal antibodies which can be employed to detect PCNA in paraffin-embedded tissues.4. Molecular biology has also been making a great contribution to the study of cell proliferation. The most recent innovation in tissue identification of proliferating cells is the use of in situ hybridization for the localization of histone H3 and/or H4 mRNA. H3 mRNA-positive cells appear to be present in basal cells of the skin and in crypt cells of the intestine which are sites with high proliferation rate.