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Biomedical subjects

L Santamaria

Publications and source records attributed to L Santamaria.

At least 19 recordsLinked to original sources
PubMed1999

Hepatic subcellular storage of beta-carotene in rats following diet supplementation.

Beta-carotene (BC) storage was measured in liver and its subcellular fractions (plasma membranes, mitochondria, microsomes and nuclei) of rats fed BC added to diet. The BC supplementation dose was about 350 mg/week/rat. After 15 weeks of this supplementation, rats were killed and their livers were immediately excised and processed to obtain total liver tissue and its subcellular fractions. Their BC contents were measured by HPLC as pmols/mg. protein Intact BC was found to be stored in all the above subcellular fractions, thus showing that BC is probably taken up by liver cell lipid moiety. Interestingly, the mean BC concentrations in plasma membranes and mitochondria were significantly higher than that in total liver tissue. Our data confirmed that rodents are a good animal model for the study of BC metabolism and its effects on several pathologies, and cancer prevention and treatment in humans in spite of the fact that rodents are classified as white-fat animals because of their poor BC absorption and storage in fat and blood plasma, whereas humans are classified as yellow-fat organisms because of their opposite behavior in BC uptake and organ distribution.

Animals↗
PubMed1996

Light and electron microscopic immunohistochemical localization of protein gene product 9.5 and ubiquitin immunoreactivities in the human epididymis and vas deferens.

The distribution of protein gene product 9.5 (PGP) and ubiquitin immunoreactivities in the ductuli efferentes, ductus epididymidis, and ductus deferens of humans was studied by Western blot analyses and light and electron microscopic immunocytochemistry. PGP immunoreactivity was intense in the ductuli efferentes and weak in the ductus epididymidis and ductus deferens, while ubiquitin immunoreactivity was intense in the ductuli efferentes and ductus epididymidis and very weak in the ductus deferens. In the ductuli efferentes epithelium, PGP immunolabeling was observed in the cytoplasm of principal cells, whereas ubiquitin immunoreactivity was found in the nucleus and cytoplasm of principal cells and ciliated cells. In the ductus epididymidis epithelium, only scattered cells (mitochondria-rich cells) showed PGP immunoreaction in their cytoplasm, whereas ubiquitin immunostaining was detected in the nucleus and cytoplasm of most epithelial cells, except for the cauda, where ubiquitin immunolabeling was observed only in the nuclei. The ductus deferens showed no immunostaining for PGP, and only nuclear immunoreactivity to ubiquitin. The ultrastructural localization of PGP immunoreactivity was in the apical cytosol and microvilli. In addition to these locations, ubiquitin immunoreactivity was also found in the nucleus of all cell types and cilia of ciliated cells. Although the distribution of PGP and ubiquitin immunoreactivities in humans differs from that reported in rats, it seems that PGP and ubiquitinated proteins are secreted into the epididymal lumen in both species.

Adult↗
PubMed1996

Carotenoids in cancer, mastalgia, and AIDS: prevention and treatment--an overview.

In 1980, two carotenoids, beta-carotene (BC) and canthaxanthine (CX) with and without pro-vitamin A activity, respectively, were orally administered to female Swiss albino mice and were found to substantially prevent skin carcinogenesis induced by benzo(a)pyrene (BP). This preventive effect was observed in darkness by means of photocarcinogenic enhancement (PCE) following UV (300 to 400 nm) irradiation. In 1984, the same experiment produced antitumorigenic activity when applied to breast carcinogenesis induced in mice by 8-methoxypsoralen (8-MOP) plus UV-A light and, in 1985, when directed toward gastric carcinogenesis induced in rats by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). These data suggested a rationale for human intervention to prevent, by carotenoid supplementation, a second primary malignancy after the primary malignancy has been radically excised. In the 1980s, a pilot clinical study (15 cases) showed a longer than expected disease-free interval in all surviving patients. It was also subsequently found that, if treated daily with 20 mg of BC and intermittently with retinol 150 to 300,000 IU daily for seven days just prior to menses, women suffering from cyclical mastalgia were relieved from pain, without any toxic side effects. When BC was given in high daily doses (60 mg) to 60 drug addicts suffering from AIDS-related complex (ARC), they recovered from their objective and subjective symptoms (but not from lymphadenopathy) with improvement in their general health and increased performance status. At higher doses, BC (with or without hyperthermia) was effective even in patients in advanced stages of AIDS. A debate has arisen concerning a recent statement by the U.S. Government that "beta-carotene supplements do not protect Americans against cancer or heart disease, and may actually increase the risk of deadly lung tumors in smokers".

Acquired Immunodeficiency Syndrome↗
PubMed1995

Whole body hyperthermia associated with beta-carotene supplementation in patients with AIDS.

The objective of this work was to check possible additive beneficial effects of whole body hyperthermia (WBH) associated with beta-carotene (BC) supplementation in patients with AIDS. In a pilot study, 10 HIV positive patients, (8 with AIDS and 2 with AIDS related complex, ARC), after AZT or DDI discontinuation, were first treated with one single session of WBH applied with a non-invasive procedure at 42 degrees C core temperature for one hour, and subsequently supplemented with BC 120 mg daily continuously. All patients well tolerated the non-invasive WBH as well as the high dose BC supplementation. Apart from one patient who died after 4 months, all the others underwent an HIV burden diminution, clinical improvement and amelioration of laboratory data, along with an subjective improvement of their life quality. With reference to control groups, namely (a) only WBH applied with extracorporeal procedure to 31 AIDS patients, and (b) only BC supplementation at high dosage applied to 64 ARC patients, the combined physical and BC supplemental treatments clearly showed a better and longer lasting response.

AIDS-Related Complex↗
PubMed1994

Giant cell formation in Hodgkin's disease.

The identity of Reed-Sternberg cells in Hodgkin's disease has remained an unresolved issue, though many studies have addressed this question. Giant cells are usually formed either by endomitosis without cytoplasmic division or by cell fusion through cytokines or viruses. Growing evidence associates Epstein-Barr virus (EBV) with Hodgkin's disease, a major issue being whether EBV is a passenger virus or has an aetiological role. This communication describes experimental conditions enabling observation of giant cell cytogenesis from peripheral blood mononuclear cells in culture. Mononuclear cells were isolated from autologous peripheral blood and cocultured with a single-cell suspension obtained from Hodgkin's lymph nodes in a culture chamber where the two cell populations are isolated by a microporous membrane that allows only cytokines and viruses to pass through. Under these experimental conditions, giant cells are formed in the peripheral blood mononuclear cell fraction; some of them appear morphologically indistinguishable from Reed-Sternberg cells and their mononuclear variant, while others much resemble Langhans giant cells. Some of these giant cells are positive for EBV DNA by in situ hybridization. These results suggest that an EBV-dependent biological activity is responsible for giant cell cytogenesis originating from lymphocytes and monocytes, induced either by EBV and/or cytokines.

Adult↗
PubMed1994

A morphological and functional assessment of Mycobacterium leprae-induced nerve damage in a guinea-pig model of leprous neuritis.

Nerve damage, resembling that caused by Mycobacterium leprae in man, was created by the injection of cobalt-irradiated M. leprae organisms into the tibial nerve of guinea-pigs. Assessment of nerve damage was made by clinical, electrophysiological and morphometric means at intervals up to 13 weeks after injection. Quantitative immunohistochemical analysis of neuropeptide-containing fibres in the skin of the foot was also carried out. Significant nerve damage occurred 3 weeks after injection of M. leprae organisms. Motor and sensory functional loss peaked at 5 weeks after injection, and there was a significant decrease of peptide-immunoreactive nerves in all skin compartments. The nerve damage was self-limiting and functional recovery had occurred by 13 weeks. The model shows many of the features found in the nerve damage of treated leprosy patients.

Animals↗
PubMed1994

Camillo Golgi as clinical pathologist: epicritical reading of Golgi's works on malaria.

Camillo Golgi confirmed, in 1885, Marchiafava's and Celli's discoveries about malaria, following a clinical-pathologic research pattern and studying the patient directly. In 1889 he associated the naturalistic-biological point of view and the clinical-pathologic one so that he made possible a differential diagnosis between tertian and quartan fever, independently from the clinical observation; he supplied useful laboratory data for clinical diagnosis and, in doing so, he created the new figure of the clinical pathologist; he distinguished three different kinds of intermittent fevers and, in 1888, he specified the useful time for quinine administration. The article analyzes, also, his methodological and scientific principles.

History, 19th Century↗
PubMed1994

Denatured muscle grafts for nerve repair in an experimental model of nerve damage in leprosy. 2. Recovery of peripheral peptide-containing nerves assessed by quantitative immunohistochemical study.

A marked depletion of neuropeptide-immunoreactive nerves, a consequence of the nerve damage which is commonly found in leprosy, has been reported in peripheral tissues of leprosy patients and of a leprosy animal model. The aim of this study was to investigate peripheral reinnervation following a denatured autologous muscle graft in an animal model of leprosy nerve damage. Possible reinnervation of the foot-pad skin was studied by immunohistochemistry using antisera to the neuronal marker protein gene product 9.5 (PGP), the neuropeptides calcitonin gene-related peptide (CGRP), substance P (SP), vasoactive intestinal peptide (VIP), and the C-flanking peptide of neuropeptide Y (CPON). The extent of the reinnervation process was assessed by image analysis quantification at different time points. At 8 weeks after muscle grafting, there were small numbers of immunoreactive nerves (p < 0.05). At 12, 16, and 20 weeks postoperatively there was a gradual increase in all immunostaining. At 20 weeks, no significant difference was found for PGP-, CGRP-, and SP-immunoreactive nerves in the epidermal and subepidermal layers compared to control (contralateral) tissue. In experimental tissue the recovery of immunoreactive nerves around sweat glands took longer (up to 12 weeks) than in other skin compartments, but after that time the recovery was rapid and at 20 weeks no difference was measured for VIP-immunoreactive nerves in comparison with controls. Around blood vessels, the recovery of CGRP- and CPON-immunoreactive fibers was slow, and at 20 weeks a difference with control samples (p < 0.01) was noted. In the same area, there was no significant difference for PGP immunoreactivity between controls and tissues at 20 weeks. In contrast, the immunoreactive nerve bundles in the dermis showed a faster recovery than nerves in other skin areas, with amounts similar to controls at 20 weeks. The significant recovery of immunoreactive nerves, in particular of those containing sensory neuropeptide, is consistent with the described functional recovery.

Animals↗
PubMed1994

beta-Carotene storage in rat organs following carrier mediated supplementation.

One rat group was supplemented with beta-carotene (BC) both in beadlets and the crystalline form in arachidic oil as a carrier added to standard diet; another rat group was given 1 ml crystalline BC-arachidic oil by gavage twice a week. In both rat groups, each rat ingested 350 mg BC/week for 12 weeks. The animals were then sacrificed and BC levels together with retinyl palmitate presence were assessed by HPLC analysis in liver, lung, kidney, small intestine, mesenteric fat, brain, spleen, stomach and blood plasma. In the first group, high BC storage, ranging from 4.2 to 45.2 nmols/g wet tissue, was found in liver, small intestine, spleen; lesser BC levels were found in lung, kidney, stomach, blood serum; retinyl palmitate was found in liver and lung. In the second group BC levels ranging from 0.5 up to 5,763 nmols/g wet tissue were detected in all organs, except for brain and stomach; the highest levels were in the lung; retinyl palmitate was detected in liver. The lung appeared to be a target organ for BC, as confirmed by its presence in the lungs of control rats fed standard diet and given 1 ml of arachidic oil alone by gavage twice a week.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Short communication: possible activity of beta-carotene in patients with the AIDS related complex. A pilot study.

In a pilot single blind study, beta-carotene (BC) supplementation produced, in ARC patients under current treatment, apparent recovery from asthenia, fever, nocturnal sweating, diarrhoea, loss in weight, and led as a result to an improvement in general health and working efficiency, but not to an improvement in multiple district lympho-adenopathies. Nevertheless, BC appeared to prevent progress to AIDS and, in addition, to lower the effective dosage of AZT used in one case of ARC developed into AIDS, producing a recovery from opportunistic infections and an inhibition of Kaposi sarcoma diffusion, in line with a two-fold rise in CD4 counts.

AIDS-Related Complex↗
PubMed1992

Carotenoids in cancer chemoprevention and therapeutic interventions.

Carotenoid (CARs: beta-carotene BC and/or canthaxanthin CX) supplementation have been shown to be chemopreventive in animals, since 1980, against direct or indirect chemical carcinogenesis/photo-carcinogenesis of the skin, breast, stomach, salivary glands, colon-rectum, urinary bladder, and against transplanted tumors. This action could be either independent of or dependent on pro-vitamin A activity of BC. In vitro, both BC and CX proved to be antimutagenic and to have anti-malignant transformation properties in cell cultures. Preliminary interventions in humans with BC +/- CX prevented the onset of second primary tumors in lung, colon, urinary bladder, and head and neck. The powerful antioxidant properties of CARs, possibly associated with their retinoid potential, played a role in all the above observations, producing free-radical quenching and immunostimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Free radicals as carcinogens and their quenchers as anticarcinogens.

An oxygen dependent signal was detected, late in the 1950s by electron spin resonance (ESR) in a saline solution of hematoporphyrin (Hp) excited by light. This signal expressed a free radical consisting of 'some kind of an association between Hp and oxygen', that Smaller et al. called 'oxyradical' (HpOO.). It soon opened a new level of understanding in carcinogenesis triggered by photodynamic substances, including Hp itself, polycyclic hydrocarbons (PCHs), as well as any carcinogen involving molecular species activated by radiation and/or metabolic reaction. Early in the 1960s, this prompted the discovery of benzo(a)pyrene (BP) photocarcinogenic enhancement (BP-PCE) in mice, probably due to an increase in free oxygen radical generation following correct light exposure. This assumption was confirmed in 1980 by the fact that mice orally loaded with antioxidants and radical quenchers, such as beta-carotene (BC) and cantaxanthin (CX), were protected against BP-PCE at 100% and against total BP carcinogenicity at more than 60%. These achievements were presented as the bases of the current explosion of interest in biology and medicine in building up the new field of chemoprevention against cancer and other chronic diseases by supplementation with antioxidant vitamins, retinoids and especially carotenoids and their synergistic association. The relevant findings of this research obtained in the last decade in in vitro and in vivo experiments as well as human interventions are reported and discussed with personal contributions.

Animals↗
PubMed1991

Identification of glucagon binding sites on smooth muscle tissue of dog intestine. Quantification by means of ultrastructural autoradiography.

125I-glucagon binding sites have been detected and quantified on the intestinal smooth muscle cells of the dog by means of ultrastructural autoradiographic methods. These binding sites are located mainly in the plasmalema. The present findings established a morphological correlation with the physiological data concerning the spasmolytic function of the glucagon on the intestinal wall.

Animals↗
PubMed1990

Photobiological effects in Saccharomyces cerevisiae induced by the monofunctional furocoumarin 4,4',6-trimethylangelicin (TMA) and the bifunctional furocoumarin 8-methoxypsoralen (8-MOP).

Recently, the monofunctional furocoumarin 4,4',6-trimethylangelicin (TMA) has been proposed for photochemotherapeutic use. In order to assess its genotoxic potential, the photobiological (genetic) effects of TMA were studied in a diploid strain of Saccharomyces cerevisiae (D7) and compared to those of the bifunctional furocoumarin 8-methoxypsoralen (8-MOP). At equimolar concentrations, the induction of lethal effects by TMA in the presence of equal 365-nm radiation was higher than that exerted by 8-MOP. TMA was also more active than 8-MOP in inducing nuclear events such as nuclear reverse mutation and mitotic recombination (crossing-overs and gene conversion) per unit dose of 365-nm radiation. At equal survival, however, TMA was less efficient in inducing reverse mutation and crossing-over, showing the same activity as 8-MOP in the induction of gene conversion. TMA was more active than 8-MOP in the induction of cytoplasmic 'petite' mutations per unit dose of 365-nm radiation and per viable cell. The high photobiological activity of this monofunctional furocoumarin is mainly related to its strong DNA photobinding but also to the type of monoaddition induced, to the sequential distribution in DNA and to the generation of active forms of oxygen.

Cell Survival↗