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Cristina Sánchez

Publications and source records attributed to Cristina Sánchez.

9 recordsLinked to original sources
PubMed2006

Factors influencing the intake and plasma levels of calcium, phosphorus and magnesium in southern Spain.

OBJECTIVE: The aim of the study was to assess factors influencing the intake and plasma levels of calcium (Ca), phosphorus (P) and magnesium (Mg) in an adult population from southern Spain, in order to identify patterns of intake and groups at risk for deficiency. METHODS: A cross-sectional survey was carried out in Andalusia, a western Mediterranean region in southern Spain. Nutrient intakes were studied in a random sample of 3,421 subjects (1,747 men, 1,674 women) between 25 and 60 years of age. Blood samples were obtained for biochemical assays in a random subsample of 354 subjects (170 men, 184 women). Food consumption was assessed by a 48-h recall. Concentrations of Ca, P and Mg were measured in plasma. Information about level of education, smoking habit, alcohol consumption and physical exercise was collected with a structured questionnaire. RESULTS: Intakes were below two-thirds of the RDA in 39.52% of the sample for Ca, and in 32.31% for Mg. Gender, age, educational level, obesity, smoking, alcohol use and physical activity were associated with differences in nutrient intakes. Plasma concentrations were below the reference value in 14.81% of the sample for Ca, and in 8.82% for Mg. Obese persons [body mass index (BMI) >/= 30 kg/m(2)] consumed less Ca, P and Mg, and had lower plasma Ca concentrations (P < 0.05) than non-obese persons. BMI showed an inverse correlation with plasma concentrations of Ca (r = -0.21, P < 0.05). CONCLUSION: Our results provide an estimate of the intake of Ca, P and Mg in the adult population of southern Spain. Of the factors that affected the intake of these nutrients, logistic regression analysis showed that only female gender and older age were associated with the risk of low plasma Ca concentrations.

Adult↗
PubMed2006

Delta9-tetrahydrocannabinol inhibits cell cycle progression in human breast cancer cells through Cdc2 regulation.

It has been proposed that cannabinoids are involved in the control of cell fate. Thus, these compounds can modulate proliferation, differentiation, and survival in different manners depending on the cell type and its physiopathologic context. However, little is known about the effect of cannabinoids on the cell cycle, the main process controlling cell fate. Here, we show that Delta(9)-tetrahydrocannabinol (THC), through activation of CB(2) cannabinoid receptors, reduces human breast cancer cell proliferation by blocking the progression of the cell cycle and by inducing apoptosis. In particular, THC arrests cells in G(2)-M via down-regulation of Cdc2, as suggested by the decreased sensitivity to THC acquired by Cdc2-overexpressing cells. Of interest, the proliferation pattern of normal human mammary epithelial cells was much less affected by THC. We also analyzed by real-time quantitative PCR the expression of CB(1) and CB(2) cannabinoid receptors in a series of human breast tumor and nontumor samples. We found a correlation between CB(2) expression and histologic grade of the tumors. There was also an association between CB(2) expression and other markers of prognostic and predictive value, such as estrogen receptor, progesterone receptor, and ERBB2/HER-2 oncogene. Importantly, no significant CB(2) expression was detected in nontumor breast tissue. Taken together, these data might set the bases for a cannabinoid therapy for the management of breast cancer.

Apoptosis↗
PubMed2006

Tumor-promoting activity of p-hydroxybenzenediazonium is accelerated in Mg-deficient rats.

Tumor-promoting activity caused by the short-term administration of p-hydroxybenzenediazonium (PDQ) has been assayed in rats fed on a Mg-deficient diet as a reference model versus rats fed on a standard diet as controls. For 5 weeks groups of 20 rats, fed either on the Mg-deficient or standard diet, were treated simultaneously with PDQ. A group of 10 Mg-deficient rats remained untreated. Topical application of PDQ was followed by the appearance of macroscopic alterations in the skin, which were more evident in the Mg-deficient rats. No deaths occurred during the treatment. After 5 weeks' PDQ treatment the rats were killed and histological analyses were made. Tissues from the skin, liver, heart, kidney, lung and thymus were screened by conventional staining methods. Both the PDQ-treated Mg-deficient and PDQ-treated control rats presented tissue lesions, although to a different extent. The untreated Mg-deficient rats showed no such lesions. Mg-deficient rats treated with PDQ developed significant incipient fibrosarcomas (p<0.05) and extended hyperplasia (p<0.001), particularly in the skin, accompanied by a significant increase in the thickness of collagen (mean value: 445.4+/-47.2microm, p<0.05) compared to the control PDQ-treated group (mean values: 258.7+/-36.4microm). The overall results provide objective proof of tumor-promoting activity after 5 weeks' treatment with PDQ. Such a fast response is interpreted as being linked to the increased vulnerability of the membrane caused by Mg deficiency, which would more readily facilitate the toxic activity of p-hydroxybenzenediazonium ions.

Animals↗
PubMed2005

Cannabinoids and ceramide: two lipids acting hand-by-hand.

Cannabinoids, the active components of Cannabis sativa (marijuana) and their endogenous counterparts, exert their effects by binding to specific G-protein-coupled receptors that modulate adenylyl cyclase and ion channels. Recent research has shown that the CB1 cannabinoid receptor is also coupled to the generation of the lipid second messenger ceramide via two different pathways: sphingomyelin hydrolysis and ceramide synthesis de novo. Sustained ceramide accumulation in tumor cells mediates cannabinoid-induced apoptosis, as evidenced by in vitro and in vivo studies. This effect seems to be due to the impact of ceramide on key cell signalling systems such as the extracellular signal-regulated kinase cascade and the Akt pathway. These findings provide a new conceptual view on how cannabinoids act, and raise interesting physiological and therapeutic questions.

Apoptosis↗
PubMed2005

Migration studies to assess the safety in use of a new antioxidant active packaging.

Both specific and overall migration tests have been applied to new experimental food packaging-active plastic films with antioxidant properties, including in its composition a natural rosemary extract. Determination of volatile and semivolatile compounds migrating from plastic to the four established simulants showed that both specific and overall migration was very low. The results obtained gave values 20 times lower than the established limits in the worst case. So, from the point of view of health risk, the new active packaging can be considered as safe. Analytical procedure used provided the necessary information about the migration behavior, with good analytical characteristics and detection limits in the sub mug kg(-1) range. Besides, no significant difference was found between laboratory and factory-made samples, which is an important issue for industrial production, the next step in the development of the new antioxidant active film.

Antioxidants↗
PubMed2004

Hypothesis: cannabinoid therapy for the treatment of gliomas?

Gliomas, in particular glioblastoma multiforme or grade IV astrocytoma, are the most frequent class of malignant primary brain tumours and one of the most aggressive forms of cancer. Current therapeutic strategies for the treatment of glioblastoma multiforme are usually ineffective or just palliative. During the last few years, several studies have shown that cannabinoids-the active components of the plant Cannabis sativa and their derivatives--slow the growth of different types of tumours, including gliomas, in laboratory animals. Cannabinoids induce apoptosis of glioma cells in culture via sustained ceramide accumulation, extracellular signal-regulated kinase activation and Akt inhibition. In addition, cannabinoid treatment inhibits angiogenesis of gliomas in vivo. Remarkably, cannabinoids kill glioma cells selectively and can protect non-transformed glial cells from death. These and other findings reviewed here might set the basis for a potential use of cannabinoids in the management of gliomas.

Animals↗
PubMed2002

De novo-synthesized ceramide is involved in cannabinoid-induced apoptosis.

Delta(9)-Tetrahydrocannabinol (THC) and other cannabinoids have been shown to induce apoptosis of glioma cells via ceramide generation. In the present study, we investigated the metabolic origin of the ceramide responsible for this cannabinoid-induced apoptosis by using two subclones of C6 glioma cells: C6.9, which is sensitive to THC-induced apoptosis; and C6.4, which is resistant to THC-induced apoptosis. Pharmacological inhibition of ceramide synthesis de novo, but not of neutral and acid sphingomyelinases, prevented THC-induced apoptosis in C6.9 cells. The activity of serine palmitoyltransferase (SPT), which catalyses the rate-limiting step of ceramide synthesis de novo, was remarkably enhanced by THC in C6.9 cells, but not in C6.4 cells. However, no major changes in SPT mRNA and protein levels were evident. Changes in SPT activity paralleled changes in ceramide levels. Pharmacological inhibition of ceramide synthesis de novo also prevented the stimulation of extracellular-signal-regulated kinase and the inhibition of protein kinase B triggered by cannabinoids. These findings show that de novo-synthesized ceramide is involved in cannabinoid-induced apoptosis of glioma cells.

Acyltransferases↗
PubMed2002

Cannabinoids and cell fate.

Cannabinoids recently have been shown to control the cell survival/death decision. Thus, cannabinoids induce growth arrest or apoptosis in a number of transformed neural and non-neural cells in culture. In addition, cannabinoid administration induces regression of malignant gliomas in rodents by a mechanism that may involve sustained ceramide generation and extracellular signal-regulated kinase activation. In contrast, most of the experimental evidence indicates that cannabinoids may protect normal neurons from toxic insults, such as glutamatergic overstimulation, ischaemia, and oxidative damage. Regarding immune cells, low doses of cannabinoids may enhance proliferation, whereas high doses of cannabinoids usually induce growth arrest or apoptosis. The potential therapeutic applications of these findings are discussed.

Animals↗