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In the scientific literature, it has been documented that electrochemical genosensors are novel analytical tools with proven clinical diagnostic potential for the identification of carcinogenic processes due to genetic and epigenetic alterations, as well as infectious diseases due to viruses or bacteria. In the present work, we describe the construction of an electrochemical genosensor for the identification of the k12p.1 mutation; it was based on use of Screen-Printed Gold Electrode (SPGE), Cyclic Voltammetry (CV), and Atomic Force Microscopy (AFM), for the monitoring the electron transfer trough the functionalized nanostructured surface and corresponding morphological changes. The sensitivity of the genosensor showed a linear response for the identification of the k12p.1 mutation of the K-ras gene in the concentration range of 10 fM to 1 µM with a detection limit of 7.96 fM in the presence of doxorubicin (Dox) as DNA intercalating agent and indicator of the hybridization reaction. Thus, the electrochemical genosensor developed could be useful for the identification of diseases related with the K-ras oncogene.
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Estrogens have been implicated in the etiology of breast cancer for a long time. It has been stated that long-term exposure to estrogens is associated with a higher incidence of breast cancer, since estradiol (E2) stimulates breast cell growth; however, its effect on DNA damage/repair is only starting to be investigated. Recent studies have documented that estrogens are able to modify the DNA damage response (DDR) and DNA repair mechanisms. On the other hand, it has been proposed that DDR machinery can be altered by estrogen signaling pathways, that can be related to cancer progression and chemoresistance. We have demonstrated that E2 promotes c-Src activation and breast cancer cell motility, through a non-genomic pathway. This review discusses scientific evidence supporting this non-genomic mechanism where estrogen modifies the DNA repair pathways, and its relationship to potential causes of chemoresistance.
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OBJECTIVE: Dental fluorosis (DF) is a dental development disorder caused by chronic fluoride overconsumption. There are differences in the susceptibility to and severity of DF in studied populations. The objective of the present study was to determine if single-nucleotide variations (SNVs) in the genes Amelogenin (AMELX), Odontogenic Ameloblast Associated (ODAM) and Matrix Metalloproteinase 20 (MMP20) are associated with DF by evaluating the relationship between variations in these genes and the degree of DF severity. SUBJECTS AND METHODS: Schoolchildren from two regions of Durango State and Mexico City, Mexico, were studied. The DF phenotype was determined using the Thylstrup and Fejerskov (TF) index. DNA was obtained from the buccal mucosa of each participant, and the presence of the variations rs946252 in AMELX, rs1514392 in ODAM and rs1784418 in MMP20 was determined by bidirectional DNA sequencing. RESULTS: A total of 180 DNA samples from 30 schoolchildren from 2 areas of Durango State were sequenced and analyzed. Differences in the severity of DF were found between the study areas (p = 0.006). SNVs in theMMP20 gene were present in 76.9 % of the participants in the high fluoride concentration and lower DF severity area. CONCLUSION: AMELX and ODAM variations was not different between the two populations with respect to DF severity; however, the presence of rs1784418 differed between phenotypes with regard to susceptibility to DF. Therefore, MMP20 might be related to the various phenotypes of DF and may serve as a protective marker.
Assuntos
Amelogenina , Fluorose Dentária , Peptídeos e Proteínas de Sinalização Intracelular , Metaloproteinase 20 da Matriz , Amelogenina/genética , Amiloide , Proteínas de Transporte , Criança , Fluoretos , Fluorose Dentária/genética , Humanos , Peptídeos e Proteínas de Sinalização Intracelular/genética , Metaloproteinase 20 da Matriz/genética , México , Proteínas de Neoplasias , Fenótipo , Análise de Sequência de DNARESUMO
Purpose: In the present study, we investigated the effects of 17ß-estradiol (E2) on membrane roughness and gold nanoparticle (AuNP) uptake in MCF-7 breast cancer cells. Methods: Estrogen receptor (ER)-positive breast cancer cells (MCF-7) were exposed to bare 20 nm AuNPs in the presence and absence of 1×10-9 M E2 for different time intervals for up to 24 hrs. The effects of AuNP incorporation and E2 incubation on the MCF-7 cell surface roughness were measured using atomic force microscopy (AFM). Endocytic vesicle formation was studied using confocal laser scanning microscopy (CLSM). Finally, the results were confirmed by hyperspectral optical microscopy. Results: High-resolution AFM images of the surfaces of MCF-7 membranes (up to 250 nm2) were obtained. The incubation of cells for 12 hrs with AuNP and E2 increased the cell membrane roughness by 95% and 30% compared with the groups treated with vehicle (ethanol) or AuNPs only, respectively. This effect was blocked by an ER antagonist (7α,17ß-[9-[(4,4,5,5,5-Pentafluoropentyl)sulfinyl]nonyl]estra-1,3,5(10)-triene-3,17-diol [ICI] 182,780). Higher amounts of AuNPs were localized inside MCF-7 cells around the nucleus, even after 6 hrs of E2 incubation, compared with vehicle-treated cells. Endolysosome formation was induced by E2, which may be associated with an increase in AuNP-uptake. Conclusions: E2 enhances AuNP incorporation in MCF-7 cells by modulating of plasma membrane roughness and inducing lysosomal endocytosis. These findings provide new insights into combined nanotherapies and hormone therapies for breast cancer.
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Neoplasias da Mama/metabolismo , Estradiol/farmacologia , Ouro/metabolismo , Nanopartículas Metálicas/química , Neoplasias da Mama/patologia , Membrana Celular/efeitos dos fármacos , Membrana Celular/metabolismo , Núcleo Celular/efeitos dos fármacos , Núcleo Celular/metabolismo , Feminino , Humanos , Células MCF-7 , Microscopia de Força Atômica , Modelos Biológicos , Receptores de Estrogênio/antagonistas & inibidores , Receptores de Estrogênio/metabolismoRESUMO
Biosensor technology has great potential for the detection of cancer through tumor-associated molecular biomarkers. In this work, we describe the immobilization of the recombinant humanized anti-HER2 monoclonal antibody (trastuzumab) on a silver nanostructured plate made by pulsed laser deposition (PLD), over a thin film of Au(111). Immobilization was performed via 4-mercapto benzoic acid self-assembled monolayers (4-MBA SAMs) that were activated with coupling reagents. A combination of immunofluorescence images and z-stack analysis by confocal laser scanning microscopy (CLSM) allowed us to detect HER2 presence and distribution in the cell membranes. Four different HER2-expressing breast cancer cell lines (SKBR3 +++, MCF-7 +/-, T47D +/-, MDA-MB-231 -) were incubated during 24 h on functionalized silver nanostructured plates (FSNP) and also on Au(111) thin films. The cells were fixed by means of an ethanol dehydration train, then characterized by atomic force microscopy (AFM) and surface-enhanced Raman scattering (SERS). SERS results showed the same tendency as CLSM findings (SKBR3 > MCF-7 > T47D > MDA-MB-231), especially when the Raman peak associated with phenylalanine amino acid (1002 cm-1) was monitored. Given the high selectivity and high sensitivity of SERS with a functionalized silver nanostructured plate (FSNP), we propose this method for identifying the presence of HER2 and consequently, of breast cancer cells.
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Proteoglycans (PGs) are essential for normal cellular development; however, alterations of their concentrations can promote tumor growth. To date, a limited number of studies report the presence of PGs in odontogenic tumors (OTs); therefore, the main purpose of this work is to gather the information published on the study of PGs. The search reported 26 articles referring to the presence of different PGs in distinct OTs from 1999 to May 2017. PGs seem to play an important role during OTs' development as they are involved in several tumor processes; however, the number of reports on the study of these molecules is low. Thus, more studies are necessary in order to gain a better understanding of the underlying pathophysiology of OTs.
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Aging is considered a systemic, chronic and low-grade inflammatory state, called "inflammaging", which has been contemplated as a risk factor for cancer development and progression in the elderly population. Cellular senescence is a multifactorial phenomenon of growth arrest and distorted function, which has been recognized as a contributor to aging. Senescent cells have an altered secretion pattern called Senescent Associated Secretory Phenotype (SASP), that comprise a complex mix of factors including cytokines, growth factors, chemokines and matrix metalloproteinases among others. The SASP secreted by accumulated senescent cells during old age has been related to local inflammation that leads to cellular transformation and therefore may be supporting the inflammaging process. Here, we evaluated if the pro-inflammatory profile within the serum obtained from elderly patients (EPS) was able to induce cellular proliferation in the breast cancer transformed cell line (MCF-7), in a similar way to the proliferation stimulated by the SASP obtained from WI-38 primary cells prematurely induced to senescence by oxidative stress (SIPS). At the same time, the participation of IL-6/IL-8 ratio was determined. Our results showed that not all the EPS increased MCF-7 proliferation. However, there was an interesting relationship between IL-6 and IL-8 concentrations, when the IL-6 was higher than IL-8. Similar results were found with SASP from SIPS-WI-38 on the MCF-7 proliferation. Although it is known that those cytokines are fundamental factors to induce proliferation; the occurrence of other components in the cellular microenvironment is necessary to carry out this effect.
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Neoplasias da Mama/metabolismo , Interleucina-6/metabolismo , Interleucina-8/metabolismo , Proteínas de Neoplasias/metabolismo , Idoso de 80 Anos ou mais , Neoplasias da Mama/patologia , Feminino , Humanos , Inflamação/sangue , Inflamação/patologia , Células MCF-7RESUMO
Fluoxetine (FLX), a selective serotonin reuptake inhibitor is an antidepressant in the treatment of mood disorders. Its impact on reproductive processes is incompletely known. The present study analyzed the reproductive effects of FLX in prepubertal female rats. Two experiments were conducted. First (acute administration), 30-day-old female rats were injected intraperitoneally with 5mg/kg of fluoxetine-hydrochloride, and were terminated 24, 48 or 72h after the treatment. Second (subchronic administration), FLX was injected on days 30-33 of age, and the animals were terminated the day of first estrus. In acute treatment estradiol concentration increased to 72h. In subchronic treatment increased serotonin concentration in ovaries and decreased the number of ova shed. An increase in number of atretic follicles and oocyte fragmentation was observed in these animals. The results suggest that FLX acts on the ovary or hypothalamus-pituitary axis resulting in modifications of the follicular development and ovulation.
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Fluoxetina/toxicidade , Oócitos/efeitos dos fármacos , Folículo Ovariano/efeitos dos fármacos , Ovário/efeitos dos fármacos , Ovulação/efeitos dos fármacos , Inibidores Seletivos de Recaptação de Serotonina/toxicidade , Serotonina/metabolismo , Fatores Etários , Animais , Feminino , Hormônios Esteroides Gonadais/sangue , Hibridização Genética , Sistema Hipotálamo-Hipofisário/efeitos dos fármacos , Sistema Hipotálamo-Hipofisário/metabolismo , Oócitos/metabolismo , Oócitos/patologia , Folículo Ovariano/metabolismo , Folículo Ovariano/patologia , Ovário/metabolismo , Ovário/patologia , Ovário/fisiopatologia , Ratos Long-Evans , Ratos Wistar , Receptor 5-HT1D de Serotonina/efeitos dos fármacos , Receptor 5-HT1D de Serotonina/genética , Receptor 5-HT1D de Serotonina/metabolismo , Maturidade Sexual , Fatores de TempoRESUMO
UNLABELLED: Ameloblastoma behavior is related to the potential of tumor cells to inhibit apoptosis and to initiate a proliferative phase. This study was performed to compare the immunoexpression of Survivin with Bcl-2, Bax, and Ki-67 and to associate them with the histopathological type of each variant of ameloblastoma. MATERIAL AND METHODS: Using the World Health Organization (WHO) criteria for ameloblastoma, 110 cases were selected. The cases were classified as solid/multicystic and unicystic ameloblastomas. Cellular counts of cytoplasmic immunoexpression were assessed for cytoplasmic Survivin, Bcl-2, and Bax, while the nuclear immunoexpression of Survivin and Ki-67 was assessed using label index. RESULTS: Cytoplasmic Survivin and Bcl-2 showed higher percentages of immunoexpression in solid multicystic ameloblastomas compared to unicystic ameloblastomas (P < 0.05). Bax, Ki-67, and nuclear Survivin were expressed in higher percentages in unicystic ameloblastomas. CONCLUSIONS: Cytoplasmic Survivin and Bcl-2 immunoexpression levels were elevated in relation to Bax immunoexpression, suggesting aggressive ameloblastoma behavior, while Ki-67 and nuclear Survivin immunoexpression may be associated with the type of tumor morphology that influences cellular counts or with the greater capacity for cellular proliferation and tumor growth.
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Ameloblastoma/metabolismo , Apoptose , Biomarcadores Tumorais/metabolismo , Proteínas Inibidoras de Apoptose/metabolismo , Neoplasias Bucais/metabolismo , Ameloblastoma/patologia , Biomarcadores Tumorais/genética , Proliferação de Células , Humanos , Proteínas Inibidoras de Apoptose/genética , Neoplasias Bucais/patologia , SurvivinaRESUMO
Tumor cells utilize inappropriate epithelial-mesenchymal transition (EMT) mechanisms during the invasive process. It is becoming increasingly clear that estradiol (E2) induces breast cancer cell progression and enhances EMT; however, the mechanisms associated with this are unclear. We investigated the role of E2 on the expression and intracellular localization of the tight junction (TJ)-associated proteins, zonula occluden 1 (ZO-1), ZO-1-associated nucleic acid binding (ZONAB), and occludin, on the activation of c-Src and human epidermal growth factor receptor 2 (HER2) expression and cellular migration in the estrogen receptor (ER)-positive breast cancer cell lines, MCF-7 and T47D. We demonstrated that 1 nM E2 elicits c-Src activation after 15 min. The p-Src/ZO-1 complex led to ZO-1 and ZONAB disruption at the TJ and increased expression of HER2 mRNAs. These changes correlate with decreased expression of the epithelial markers occludin and CRB3 and increased synthesis of N-cadherin. This led to increased MCF-7 cell migration induced by E2, even in the presence of a cell proliferation inhibitor. Incubation with ICI 182,780 (Fulvestrant), an ER antagonist, precluded the effects of E2 on c-Src phosphorylation, p-Src/ZO-1 complex formation, ZO-1/ZONAB nuclear translocation, and migration of MCF-7 cells. Our findings suggest that E2 promotes TJ disruption during tumor progression and increases cell motility. We propose a novel pathway where estrogens promote EMT-associated mechanisms that possibly lead to metastasis.
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Neoplasias da Mama/patologia , Transição Epitelial-Mesenquimal , Estradiol/farmacologia , Transdução de Sinais/fisiologia , Junções Íntimas/fisiologia , Transporte Ativo do Núcleo Celular , Proteína Tirosina Quinase CSK , Caderinas/análise , Linhagem Celular Tumoral , Movimento Celular/efeitos dos fármacos , Feminino , Humanos , Receptores de Estrogênio/fisiologia , Proteína da Zônula de Oclusão-1/metabolismo , Quinases da Família src/metabolismoRESUMO
The effects of an electric current on growth and hexadecane (HXD) degradation by Aspergillus niger growth were determined. A 450-mL electrochemical cell with titanium ruthenium-oxide coated electrodes and packed with 15 g of perlite (inert biomass support) was inoculated with A. niger (2.0×10(7) spores (g of dry inert support)(-1)) and incubated for 12 days (30 °C; constant ventilation). 4.5 days after starting culture a current of 0.42 mA cm(-2) was applied for 24h. The current reduced (52±11%) growth of the culture as compared to that of a culture not exposed to current. However, HXD degradation was 96±1.4% after 8 days whereas it was 81±1.2% after 12 days in control cultures. Carbon balances of cultures not exposed to current suggested an assimilative metabolism, but a non-assimilative metabolism when the current was applied. This change can be related to an increase in total ATP content. The study contributes to the knowledge on the effects of current on the mycelial growth phase of A. niger, and suggests the possibility of manipulating the metabolism of this organism with electric current.
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Alcanos/metabolismo , Aspergillus niger/crescimento & desenvolvimento , Aspergillus niger/metabolismo , Biomassa , Eletricidade , Modelos Biológicos , Trifosfato de Adenosina/metabolismo , Biodegradação Ambiental , Carbono/análise , Dióxido de Carbono/metabolismo , Técnicas Eletroquímicas , Concentração de Íons de Hidrogênio , Consumo de Oxigênio , Fatores de TempoRESUMO
BACKGROUND AND AIMS: Syndecan-1 (SDC-1) is a member of the family of transmembrane heparan sulfate proteoglycans, which are involved in cell-cell adhesion and the interaction of cells with the extracellular matrix. Evidence suggests that loss of SDC-1 expression in several benign and malignant epithelial neoplasms is an unfavorable prognostic indicator, but its expression profile in thyroid gland neoplasms remains to be elucidated. The aim of this study was to evaluate SDC-1 expression in papillary carcinomas of the thyroid (PCT) that were both larger and smaller (papillary microcarcinoma) than 10mm, with or without extracapsular extension (PCT-E and PCT-NE). METHODS: The expression of SDC-1 was studied in 62 cases of PCT-E and PCT-NE using a tissue microarrays technique (TMA). SDC-1 positivity was predominantly observed in the cytoplasm of neoplastic epithelial cells and in the stroma of PCT. RESULTS: SDC-1 is expressed in both neoplastic epithelial cells and the stroma. It is more frequently expressed in PCT-E than PCT-NE (p=0.002) and the stromal expression of SDC-1 is more intense in PCT-E that are >10 mm (p=0.026). CONCLUSIONS: The epithelial and stromal expression of SDC-1 observed in this series of PCT suggests that the expression of this protein may be related to extracapsular invasion.
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Carcinoma Papilar/metabolismo , Invasividade Neoplásica , Sindecana-1/metabolismo , Neoplasias da Glândula Tireoide/metabolismo , Adolescente , Adulto , Idoso , Carcinoma Papilar/patologia , Feminino , Humanos , Imuno-Histoquímica , Masculino , Pessoa de Meia-Idade , Neoplasias da Glândula Tireoide/patologia , Adulto JovemRESUMO
The aims of the present study were to examine whether the pattern of syndecan-1 expression correlates with cellular proliferation index in desmoplastic ameloblastomas (DA), peripheral ameloblastomas (PA) and ameloblastic carcinomas (AC), and to compare with that previously reported for solid (SA) and unicystic (UA) variants of ameloblastoma. Immunohistochemistry was performed for syndecan-1 and Ki-67 in seven ameloblastomas (four DA and three PA) and three AC. Expression of syndecan-1 was related to the histological subtype of tumors and, in the case of malignancy, to lower expression levels observed in AC (22.5%) than in PA (47.5%) or DA (77.5%) (P < 0.05). Syndecan-1 expression correlated inversely with Ki-67 proliferative index: the expression was lower in both types of ameloblastomas (1.5% in DA and 6.4% in PA) than in AC (41.2%; P < 0.05). The present results suggest that the decrease in syndecan-1 expression and increase in the Ki-67 index observed in AC is in accordance with its higher aggressiveness as compared to the rare DA and PA. Interestingly, DA had a lower proliferation index as well as the highest levels of syndecan-1 expression. These data suggest that DA differ from the other types of intraosseous ameloblastomas but more studies are necessary to better understand the role of this protein as a marker in the biological behavior of the epithelial odontogenic neoplasms.
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Ameloblastoma/patologia , Carcinoma/patologia , Neoplasias Maxilomandibulares/patologia , Antígeno Ki-67/biossíntese , Sindecana-1/biossíntese , Ameloblastoma/metabolismo , Carcinoma/metabolismo , Proliferação de Células , Humanos , Imuno-Histoquímica , Neoplasias Maxilomandibulares/metabolismo , PrognósticoRESUMO
Aging is a process where individuals decrease the performance of their physiological systems and cellular stress response, making them more susceptible to disease and death. The increase in DNA damage associated with age might be recognized as the accumulation of physiological and environmentally induced mutations accompanied with a decline in DNA repair. DNA mismatch repair (MMR) is the main postreplicative correction pathway, which is known to decrease with age. However, since infrequent occurrence of direct DNA damage contrasts with the extensive cell and tissue dysfunction seen in older individuals, the withdrawing of DNA-repairing systems might be also related to epigenetic changes, such as DNA methylation. It has been reported that the physiological stress related to breeding might accelerate the acquisition of aging-related markers; therefore, the aim of this work was to link age with epigenetic modifications in this animal population. Hence, the correlation of Msh2 gene silencing with the deterioration of breeding female mice associated to aging was determined. Combined bisulfite restriction analysis assay was used to compare methylation on DNA isolated from twelve-month-old retired breeders against nulliparous female mice aged-matched, and two-month-old young adults. Our experiments clearly reveal Msh2 promoter hypermethylation associated to the aging process. A higher degree methylation was additionally observed in breeding females DNA. Nevertheless, this additional methylation did not correlate with a further decrease Msh2 mRNA, suggesting that the increase in methylation in old retired breeder might account for further epigenetic changes that could additionally promote the aging process.
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Envelhecimento , Marcadores Genéticos/genética , Proteína 2 Homóloga a MutS/genética , Regiões Promotoras Genéticas , Reprodução/fisiologia , Envelhecimento/patologia , Envelhecimento/fisiologia , Animais , Cruzamento , Dano ao DNA , Metilação de DNA , Reparo do DNA , Epigênese Genética , Feminino , Camundongos , Proteína 2 Homóloga a MutS/metabolismoRESUMO
The role played by the serotoninergic system in the control of puberty onset and first ovulation in rats is studied in this paper by analyzing the effects of injecting the neurotoxin 5,6-dihydroxytryptamine (5,6-DHT) into the dorsal (DRN) or medial (MRN) raphe nucleus of 30-day-old female rats. Complete lesion to the DRN resulted in the blockade of ovulation and a decrease in both the number of ovarian follicles and the serum concentration of follicle stimulating hormone (FSH). This treatment was also found to be associated with an increase in serotoninergic activity in the anterior and medial hypothalami. A lesion to the central portion of the DRN resulted in a significant decrease in the concentration of progesterone in serum and in the number of ova shed by ovulating animals. The lesion to the lateral portion of the DRN did not have an apparent effect on ovulation rate, the number of ova shed, nor in hormone serum concentration. The injection of propranolol to rats with a lesion to the DRN restored ovulation in 73% of treated animals and returned serotoninergic activity in the anterior hypothalamus to levels similar to those of sham-operated animals. In turn, in the medial hypothalamus, the increase in serotoninergic activity was not modified. The results presented herein suggest that serotoninergic inputs to the anterior hypothalamus have a direct influence on gonadotropin secretion and first ovulation, while the noradrenergic innervation exerts an indirect influence.
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5,6-Di-Hidroxitriptamina/administração & dosagem , Núcleo Mediodorsal do Tálamo/efeitos dos fármacos , Núcleos da Rafe/efeitos dos fármacos , Serotoninérgicos/administração & dosagem , 5,6-Di-Hidroxitriptamina/farmacologia , Antagonistas Adrenérgicos beta/farmacologia , Animais , Mapeamento Encefálico , Estradiol/sangue , Estro/efeitos dos fármacos , Estro/metabolismo , Feminino , Hormônio Foliculoestimulante/sangue , Ácido Hidroxi-Indolacético/metabolismo , Hipotálamo/efeitos dos fármacos , Hipotálamo/metabolismo , Hormônio Luteinizante/metabolismo , Núcleo Mediodorsal do Tálamo/fisiologia , Folículo Ovariano/efeitos dos fármacos , Folículo Ovariano/metabolismo , Folículo Ovariano/fisiopatologia , Ovulação/efeitos dos fármacos , Ovulação/metabolismo , Progesterona/sangue , Propranolol/farmacologia , Núcleos da Rafe/anatomia & histologia , Núcleos da Rafe/fisiologia , Ratos , Ratos Endogâmicos , Serotoninérgicos/farmacologia , Vagina/efeitos dos fármacos , Vagina/metabolismoRESUMO
The mechanism of cadmium-mediated hepatotoxicity has been the subject of numerous investigations, principally in hepatocytes. Although, some uncertainties persist, sufficient evidence has emerged to provide a reasonable account of the toxic process in parenchymal cells. However, there is no information about the effect of cadmium in other hepatic cell types, such as stellate cells (fat storing cells, Ito cells, perisinusoidal cells, parasinusoidal cells, lipocytes). Hepatic stellate cells (HSC) express a quiescent phenotype in a healthy liver and acquire an activated phenotype in liver injury. These cells play an important role in the fibrogenic process. The objective of this study was to investigate the effect of a 24 h treatment of low Cd concentrations in glutathione content, lipid peroxidation damage, cytosolic free Ca, antioxidant enzyme activities: glutathione peroxidase, glutathione reductase, superoxide dismutase and catalase along with the capacity of this heavy metal to induce metallothionein II and alpha(1)collagen (I) in an hepatic stellate cell line (CFSC-2G). Cd-treated cells increased lipid peroxidation and the content of cytosolic free calcium, decreased glutathione content and superoxide dismutase, glutathione peroxidase and catalase activity. Cd was able to induce the expression of the metallothionein II and alpha(1)collagen (I) gene, that was not described in this cell type. Cadmium may act as a pro-fibrogenic agent in the liver probably by inducing oxidative damage by enhancing lipid peroxidation and altering the antioxidant system of the cells. Although, the exact role metallothionein induction plays in this process is unknown, it probably, provides a cytosolic pool of potential binding sites to sequester ionic Cd, thereby decreasing its toxicity.