PubMed Health⌕ Search

Biomedical subjects

J J Garcia

Publications and source records attributed to J J Garcia.

At least 19 recordsLinked to original sources

Effect of the preventive-therapeutic administration of melatonin on mammary tumour-bearing animals.

Melatonin has been reported to be involved in the feedback between neuroendocrine and immune functions and to exert oncostatic actions. Likewise, this hormone seems to lengthen life span in healthy animals. As of present, most studies have analysed the therapeutic effect of melatonin on cancer growth, but few have tested the preventive effect of melatonin in reducing the risk of cancer. Thus, the aim of this study was to evaluate the preventive-therapeutic effects of melatonin on rats with DMBA-induced mammary tumours, and to examine the effect of melatonin on the first line of cell defence against cancer (macrophages and NK cells) and on some of the neuroendocrine factors that are involved in the development of tumours (prolactin and catecholamines). Melatonin treatment (5 mg/day/animal) began one month prior to DMBA (9,10-dimethyl-1,2-benzanthracene) administration to females Sprague Dawley rats. It was found that the treatment led to an increase in survival and in latency time in the tumour-bearing rats. Although the melatonin treatment did not influence either the phagocytic capacity of macrophages or the number of peripheral blood NK cells, it did stabilise the levels of prolactin by returning the concentrations of this hormone to those of the healthy animals. We conclude that melatonin can exert an oncostatic action, lengthening the survival time of mammary tumour-bearing animals, and suggest that this effect is due, at least in part, to regulating the neuroendocrine parameters of tumour-bearing animals, bringing them closer to their optimal physiological status.

Adjuvants, Immunologic↗

Melatonin increases the survival time of animals with untreated mammary tumours: neuroendocrine stabilization.

The aim of this study was to evaluate the therapeutic effect of melatonin, the main hormone of the pineal gland, on rats with advanced and untreated mammary tumours. Mammary tumours were chemically induced in Sprague-Dawley rats with the carcinogen 9,10-dimethyl-1,2-bezanthracene (DMBA). After the appearance of tumours the effect of melatonin (5 mg/ml per rat per day) was then evaluated on the survival time, tumour multiplicity, and tumour volume until the death of the animals. In addition, the variations in prolactin, noradrenaline and adrenaline concentrations, and in the percentage of NK cells were evaluated after one month of the treatment with melatonin. Daily administration of melatonin increased significantly the survival time of tumour-bearing animals (p<0.05 with respect to the control non-melatonin-receiving rats). The increased survival time did not correlate, however, with changes in either tumour multiplicity or tumour growth rate. Animals with mammary tumours exhibited an increase (p<0.05 with respect to healthy animals) in prolactin and catecholamine concentrations. The administration of melatonin stabilized the hormone levels, returning them to those in the basal-healthy animals. Rats with mammary tumours also presented lower percentages of NK cells, which were not increased by the administration of melatonin. The results strongly suggest that melatonin per se is beneficial during advanced breast cancer. It increases survival time, maybe by improving the homeostatic and neuroendocrine equilibrium which is imbalanced during advanced breast cancer.

9,10-Dimethyl-1,2-benzanthracene↗

Comparison of the protective effect of melatonin with other antioxidants in the hamster kidney model of estradiol-induced DNA damage.

17beta-Estradiol (E(2)) is a known carcinogen. Estrogen induction of tumors in hamster kidney is a model of estrogen-related carcinogenesis. Melatonin is a well-known antioxidant, free radical scavenger and oncostatic agent. Changes in the levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodGuo), an index of DNA damage, were measured in kidneys, liver and testes from hamsters treated with E(2) (75mg/kg b.w.) and collected 5h later. Potential protective effects of melatonin, N-acetylserotonin (NAS), indole-3-propionic acid (IPA) and ascorbic acid (AA) against E(2)-induced DNA damage were tested. The antioxidants were applied in equimolar doses of 64.5 micromol/kg b.w., 2 and 0.5h before and 2 and 4h after E(2) treatment. E(2) treatment caused a significant increase in 8-oxodGuo levels in kidneys, but did not influence significantly the oxidation of guanine bases in liver and testes. Melatonin, IPA and AA, but not NAS, completely prevented E(2)-induced DNA damage in hamster kidneys. It is concluded that melatonin, IPA and AA may be effective in protecting against E(2)-related DNA damage and, consequently, carcinogenesis.

Animals↗

Epizootiological studies of Amblyospora albifasciati (Microsporidiida: Amblyosporidae) in natural populations of Aedes albifasciatus (Diptera: Culicidae) and Mesocyclops annulatus (Copepoda: Cyclopidae) in a transient floodwater habitat.

The epizootiology of the microsporidium Amblyospora albifasciati was studied in natural populations of its definitive host, a multivoltine, neotropical, floodwater mosquito, Aedes albifasciatus, and its intermediate copepod host, Mesocyclops annulatus, in an ephemeral floodwater habitat during a 12-month period. A. albifasciati was enzootic in mosquitoes. Vertically (transovarially) transmitted meiospore infections occurred regularly and were detected in five of eight larval broods but the prevalence of infection was always low, ranging from 0.5 to 6.9% with an overall average of 0.7%. Horizontal transmission of A. albifasciati infection from copepods to mosquitoes was nominal and limited. It was detected at levels of 6.4 to 20% in larval Ae. albifasciatus populations on two occasions, the month of August and late September through early October. The low levels of horizontal transmission of infection to mosquito larvae appeared to be the principal limiting factor that prevented the proliferation of A. albifasciati in Ae. albifasciatus populations. Copepod populations were abundant from May through September and weekly prevalence rates of A. albifasciati averaged over 50% (range = 5.8 to 100%). The moderately high infection rates in M. annulatus copepods were inconsistent with the low prevalence of meiospore infection in Ae. albifasciatus mosquito larvae. Results suggest that either meiospores of A. albifasciati produced in the mosquito host are highly infectious to copepods or they are long-lived and remain viable within the pool as long as some standing water is present. Observations further indicate that A. albifasciati has a significant detrimental impact on M. annulatus copepod populations but minimal impact on larval populations of Ae. albifasciatus at this site.

Aedes↗

Primary and continuous midgut cell cultures from Pseudaletia unipuncta (Lepidoptera: Noctuidae).

Midgut epithelial cells were isolated from fifth-instar Pseudaletia unipuncta larvae by collagenase treatment of midgut tissue, and cultured in TNM-FH medium. Long-term continuous culture and maintenance of midgut cells were achieved with P. unipuncta armyworm intestinal cells. Several cells lines were obtained from these P. unipuncta primary cultures, and they have been subcultured and maintained for over 24 mo. The three major midgut cell types were present in the cultures, including stem (regenerative), columnar, and goblet cells. In vitro morphogenesis and differentiation of columnar and goblet cells from stem cells were observed. There appeared to be a cycle of cell death of goblet and columnar cells followed by their replacement from stem cells every 7-8 wk. After approximately six passages, the cell density in T-flasks appeared to be somewhat constant, reaching 10(3)-10(4) cells per milliliter of medium. The columnar cells are round to rectangular in shape and possess a brush border, while the goblet cells have a classic flask-like shape with a central cavity. Peritrophic membrane-like secretions were observed in all the culture flasks. Infection of these cells with multiply embedded nucleopolyhedrovirus was confirmed, and we conclude that these midgut cells can be used as an in vitro model system to study early events in baculovirus infection.

Animals↗

Carcinogen-induced, free radical-mediated reduction in microsomal membrane fluidity: reversal by indole-3-propionic acid.

Chromium (Cr) is a well established carcinogen, with Cr(III) accounting for much of the intracellular oxidative damage that this transition metal induces. Indole-3-propionic acid (IPA), a melatonin-related molecule, is a reported antioxidant and free radical scavenger. Concentration (1, 10, 100, 500, or 1000 microM) and time (15, 30, 45, 60, or 90 min)-dependent effects of Cr(III) in the presence of H2O2 (0.5 mM), as well as the protective effect of IPA on Cr(III)-induced alterations in membrane fluidity (the inverse of membrane rigidity), as an index of membrane damage, were estimated by fluorescence spectroscopy. Cr(III), in a concentration- and a time-dependent manner, decreased membrane fluidity, with marked effects at a concentration of 500 microM and 60 min of incubation. IPA (5, 3, or 1 mM) prevented the Cr(III)-induced decrease in membrane fluidity. It is concluded that the carcinogen Cr(III), in the presence of H202, generates free radicals, which decrease membrane fluidity in rat microsomal membranes. Membrane alterations are pharmacologically prevented by the antioxidant IPA.

Animals↗

Effects of ispaghula husk and guar gum on postprandial glucose and insulin concentrations in healthy subjects.

OBJECTIVE: The aim of this study was to evaluate, under the same experimental conditions and in the same subjects, the effects of ispaghula husk and guar gum on postprandial glucose and insulin concentrations in healthy female subjects. DESIGN: An oral glucose load with and without fiber was administered in the morning after an overnight fast. The study of the fiber effect was planned according to a randomized and cross-over design. SETTING: The study was performed at the Department of Pharmacology, Toxicology and Nursing at the University of León (Spain). SUBJECTS: Ten healthy female volunteers aged 30-48 y with normal body mass indices participated in this study. RESULTS: A significant decrease in mean serum insulin concentrations was observed from 30 to 90 min in the presence of both fibers. The area under the insulin curve was significantly reduced by 36.1% for ispaghula husk and 39.4% for guar gum. The area under the glucose curve was reduced by 11.1% (significant difference) for ispaghula husk and 2.6% for guar gum (no significant difference). CONCLUSIONS: According to the results obtained in this study, the administration of ispaghula husk may be beneficial due to its ability to reduce glucose postprandial concentration and especially insulin requirements. Individualization of the treatment would be advisable due to large individual variations observed in glycemic and insulinemic postprandial responses.

Adult↗

Indole-3-propionic acid, a melatonin-related molecule, protects hepatic microsomal membranes from iron-induced oxidative damage: relevance to cancer reduction.

Excessive free iron and the associated oxidative damage are commonly related to carcinogenesis. Among the antioxidants known to protect against iron-induced oxidative abuse and carcinogenesis, melatonin and other indole compounds recently have received considerable attention. Indole-3-propionic acid (IPA), a deamination product of tryptophan, with a structure similar to that of melatonin, is present in biological fluids and is an effective free radical scavenger. The aim of the study was to examine the effect of IPA on experimentally induced oxidative changes in rat hepatic microsomal membranes. Microsomes were preincubated in presence of IPA (10, 3, 2, 1, 0.3, 0.1, 0.01 or 0.001 mM) and, then, incubated with FeCl(3) (0.2 mM), ADP (1.7 mM) and NADPH (0.2 mM) to induce oxidative damage. Alterations in membrane fluidity (the inverse of membrane rigidity) were estimated by fluorescence spectroscopy and lipid peroxidation by measuring concentrations of malondialdehyde+4-hydroxyalkenals (MDA+4-HDA). IPA, when used in concentrations of 10, 3 or 2 mM, increased membrane fluidity, although at these concentrations it did not influence lipid peroxidation significantly. The decrease in membrane fluidity due to Fe(3+) was completely prevented by preincubation in the presence of IPA at concentrations of 10, 3, 2 or 1 mM. The enhanced lipid peroxidation due to Fe(3+) was prevented by IPA only at the highest concentration (10 mM). It is concluded that Fe(3+)-induced rigidity and, to a lesser extent, lipid peroxidation in microsomal membranes may be reduced by IPA. However, IPA in high concentrations increase membrane fluidity. Besides melatonin, IPA may be used as a pharmacological agent to protect against iron-induced oxidative damage to membranes and, potentially, against carcinogenesis.

Adenosine Diphosphate↗

Protein binding of glipizide using equilibrium dialysis technique: effects of hydrogen ion concentration, drug concentration and ionic strength.

The objective of this research was to investigate the effects of hydrogen ion concentration, drug concentration and ionic strength on the binding affinity of glipizide to albumin protein. Different buffer solutions of different pH values (pH 6.7, 7.5 and 8.5), different drug concentrations (2.45 mg, 4.82 mg and 9.42 mg), and phosphate buffer solutions pH 7.5 of different ionic strength (0.1, 0.4 and 1.0) were prepared. The effects of pH, drug concentration and ionic strength on the amount of glipizide bounded to 0.25 g bovine albumin was investigated. As the pH of the solution was increased from pH 6.4 to pH 8.5, milligrams drug bounded to gram protein (r value) decreased from 8.2 mg to 3.84 mg/g protein. Also as the ionic strength of the solution was increased from 0.1 to 1.0, the r value decreased from 10.76 mg to 3.96 mg/g protein. However, the r value did not change significantly with increasing of drug from 2.45 mg to 9.42 mg/25 ml. The r value was 7.36 mg/g protein when concentration of the drug was 2.45 mg/25 ml and 7.4 mg/g protein when the concentration of the drug was 9.42 mg/25 ml. This study demonstrated that factors such as high pH and high ionic strength can alter drug-protein binding and consequently increase free drug in plasma and increase bioavailability of slightly water insoluble drug such as antidiabetic drugs.

Dialysis↗

Melatonin reduces rat hepatic macromolecular damage due to oxidative stress caused by delta-aminolevulinic acid.

Delta-aminolevulinic acid, precursor of heme, accumulates in a number of organs, especially in the liver, of patients with acute intermittent porphyria. The potential protective effect of melatonin against oxidative damage to nuclear DNA and microsomal and mitochondrial membranes in rat liver, caused by delta-aminolevulinic acid, was examined. Changes in 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels, an index of DNA damage, and alterations in membrane fluidity (the inverse of membrane rigidity) and lipid peroxidation in microsomal and mitochondrial membranes, as indices of damage to lipid and protein molecules in membranes, were estimated. Measurements were made in rat liver after a 2 week treatment with delta-aminolevulinic acid (40 mg/kg b.w., every other day). To test the potential protective effects of melatonin, the indole was injected (i.p. 10 mg/kg b.w.) 3 times daily for 2 weeks. 8-OHdG levels and lipid peroxidation in microsomal membranes increased significantly whereas microsomal and mitochondrial membrane fluidity decreased as a consequence of delta-aminolevulinic acid treatment. Melatonin completely counteracted the effects of delta-aminolevulinic acid. Melatonin was highly effective in protecting against oxidative damage to DNA as well as to microsomal and mitochondrial membranes in rat liver and it may be useful as a cotreatment in patients with acute intermittent porphyria.

8-Hydroxy-2'-Deoxyguanosine↗

Melatonin reduces oxidative neurotoxicity due to quinolinic acid: in vitro and in vivo findings.

The in vivo and in vitro effects of melatonin on quinolinic acid-induced oxidative damage in rat brain were determined. The concentrations of malonaldehyde and 4-hydroxyalkenals were assayed as an index of oxidatively damaged lipid. In in vitro experiments, the increase in malonaldehyde and 4-hydroxyalkenals concentrations induced by quinolinic acid were concentration-dependent and time-dependent. The accumulation of products of lipid peroxidation induced by quinolinic acid were very significantly reduced by melatonin in a concentration-dependent manner. Additionally, at the highest concentrations of melatonin used in quinolinic acid treated homogenates, it reduced the levels of oxidatively damaged lipid products below those measured in control homogenates (no quinolinic acid or melatonin). When quinolinic acid (200 mg/kg) was intraperitonally injected into 11-day-old rats, lipid peroxidation in the brain was significantly increased 24 hours later compared to levels in control rats. When melatonin (10 mg/kg) was injected i.p. 30 min before and 4 and 20 hours after the administration of quinolinic acid, the increased lipid peroxidation induced by quinolinic acid was significantly reduced. Likewise, neurobehavioral signs associated with quinolinate administration were attenuated by melatonin. These results show that both in vitro and in vivo pharmacological levels of melatonin confer protection against quinolinic acid-induced oxidative toxicity in the brain. The findings also indicate that melatonin may be pharmacologically useful in combatting quinolinic neurotoxicity which is associated with several acute and chronic neurodegenerative neurological diseases.

Animals↗

Melatonin reduces phenylhydrazine-induced oxidative damage to cellular membranes: evidence for the involvement of iron.

Phenylhydrazine and iron overload result in augmented oxidative damage and an increased likelihood of cancer. Melatonin is a well known antioxidant and free radical scavenger. The aim of this study was to determine whether melatonin would protect against phenylhydrazine-induced oxidative damage to cellular membranes and to evaluate the possible role of iron in this process. Changes in lipid peroxidation and microsomal membrane fluidity were estimated after the treatment of rats with phenylhydrazine (15 mg/kg body weight, daily, 7 days) alone and melatonin or ascorbic acid (15 mg/kg body weight, two times daily, 8 days), or their combination. Additionally, lipid peroxidation was measured in liver homogenates from untreated and melatonin or ascorbic acid-treated rats in vivo and exposed to iron in vitro. Melatonin, but not ascorbic acid, reduced phenylhydrazine-induced lipid peroxidation in vivo in spleen (3.16+/-0.06 vs. 3.83+/-0.12 nmol/mg protein, P<0.05) and plasma (7. 73+/-0.52 vs. 9.96+/-0.71 nmol/ml, P<0.05) and attenuated the decrease in hepatic microsomal membrane fluidity (1/polarization, 3. 068+/-0.007 vs. 3.027+/-0.008, P<0.05). In vitro exposure to iron significantly enhanced the lipid peroxidation in liver homogenates from untreated (3.34+/-0.75 vs. 1.25+/-0.28, P<0.05) or ascorbic acid-treated rats (2.72+/-0.39 vs. 0.88+/-0.06, P<0.05) but not from melatonin-treated rats (1.49+/-0.55 vs. 0.68+/-0.20, NS). It is concluded that free radical mechanisms are involved in the toxicity of phenylhydrazine and that the antioxidant melatonin, but not ascorbic acid, reduces the toxic affects of phenylhydrazine in vivo and of iron in vitro in cell membranes. Therefore, melatonin co-treatment in conditions of iron overload may prove beneficial.

Animals↗

Protective effects of melatonin against oxidation of guanine bases in DNA and decreased microsomal membrane fluidity in rat liver induced by whole body ionizing radiation.

The aim of the study was to examine the potential protective effect of melatonin against whole body ionizing radiation (800 cGy). Changes in 8-hydroxy-2'-deoxyguanosine (8-OH-dG) levels, an index of DNA damage, and alterations in membrane fluidity (the inverse of membrane rigidity) and lipid peroxidation in microsomal membranes, as indices of damage to lipid and protein molecules in membranes, were estimated. Measurements were made in rat liver, 12 h after their exposure to radiation. To test the potential protective effects of melatonin, the indole was injected (i.p. 50 mg/kg b.w.) at 120, 90, 60 and 30 min prior to radiation exposure. Both 8-OH-dG levels and microsomal membrane rigidity increased significantly 12 h after radiation exposure. Melatonin completely counteracted the effects of ionizing radiation. Changes in 8-OH-dG levels and membrane fluidity are early sensitive parameters of DNA and microsomal membrane damage, respectively, induced by ionizing radiation and our findings document the protective effects of melatonin against ionizing radiation.

8-Hydroxy-2'-Deoxyguanosine↗

Increased levels of oxidatively damaged DNA induced by chromium(III) and H2O2: protection by melatonin and related molecules.

Chromium (Cr) compounds are known occupational and environmental carcinogens. This trace element is found in the workplace primarily in the valence forms Cr(III) and Cr(VI). Cr(III), which was thought originally to be relatively nontoxic, was recently found to be more reactive toward purified DNA than was chromium(VI). Herein, we examined the ability of Cr(III) to induce oxidative DNA damage by measuring the formation of 8-hydroxydeoxyguanosine (8-OH-dG) in purified calf thymus DNA incubated with CrCl3 plus H2O2. In this system we observed that the Cr(III)-induced formation of 8-OH-dG in isolated DNA was both dose- and time-dependent. When melatonin and related molecules, including 6-methoxy-1,2,3,4-tetrahydro-beta-carboline (pinoline), N-acetylserotonin, 6-hydroxymelatonin and indole-3-propionic acid, were co-incubated with CrCl3 plus H2O2, the accumulations of 8-OH-dG in DNA samples were markedly inhibited in a concentration-dependent manner. The concentrations of each indole required to reduce DNA damage by 50%, i.e. the IC50 values, were 0.48, 0.51, 0.88, 1.00 and 3.08 microM for pinoline, melatonin, N-acetylserotonin, 6-hydroxymelatonin and indole-3-propionic acid, respectively. These results suggest that one of the mechanisms by which Cr(III) may induce cancer is via Fenton-type reactions which generate the hydroxyl radical (*OH). The findings also indicate that the protective effects of melatonin and related molecules against Cr(III)-induced carcinogenesis relate to their direct *OH scavenging ability which thereby reduces the formation of the damaged DNA product, 8-OH-dG.

8-Hydroxy-2'-Deoxyguanosine↗

Estimation of in situ elastic properties of biphasic cartilage based on a transversely isotropic hypo-elastic model.

Articular cartilage is known to behave nonlinearly for large deformations. Mechanical properties derived from small strain experiments yield excessively large deformations in finite element models used in the study of severe blunt impact to joints. In this manuscript, a method is presented to determine the nonlinear elastic properties of biphasic cartilage based on a transversely isotropic hypo-elastic model. The elastic properties were estimated by fitting two force-displacement curves (in rapid loading and at equilibrium) obtained from large deformation indentation relaxation tests on cartilage using a nonporous spherical indentor. The solid skeleton of the cartilage was modeled as a transversely isotropic hypo-elastic material and a commercial finite element program was employed to solve the problem of a layer indented by a rigid sphere. Components of the hypo-elasticity tensor were made dependent on deformation according to the variations defined by a transversely isotropic hyperelastic formulation given earlier by others. Material incompressibility was assumed during the initial stage of rapid loading. The analysis was utilized for the determination of in situ properties of rabbit retropatellar cartilage at large deformations. The model was able to fit the material response to rapid loading and equilibrium indentation test data to approximately 50 percent strain. This material model suggested even higher percentage of stress supported by the fluid phase of cartilage than given earlier by small deformation theories of biphasic cartilage.

Animals↗

Chromium(III)-induced 8-hydroxydeoxyguanosine in DNA and its reduction by antioxidants: comparative effects of melatonin, ascorbate, and vitamin E.

Chromium compounds are well documented carcinogens. Cr(III) is more reactive than Cr(VI) toward DNA under in vitro conditions. In the present study, we investigated the ability of Cr(III) to induce oxidative DNA damage by examining the formation of 8-hydroxydeoxyguanosine (8-OH-dG) in calf thymus DNA incubated with CrCl(3) plus H(2)O(2). We measured 8-OH-dG using HPLC with electrochemical detection. In the presence of H(2)O(2), we observed that Cr(III)-induced formation of 8-OH-dG in isolated DNA was dose and time dependent. Melatonin, ascorbate, and vitamin E (Trolox), all of which are free radical scavengers, markedly inhibited the formation of 8-OH-dG in a concentration-dependent manner. The concentration that reduced DNA damage by 50% was 0.51, 30.4, and 36.2 microM for melatonin, ascorbate, and Trolox, respectively. The results show that melatonin is 60- and 70-fold more effective than ascorbate or vitamin E, respectively, in reducing oxidative DNA damage in this in vitro model. These findings also are consistent with the conclusion that the carcinogenic mechanism of Cr(III) is possibly due to Cr(III)-mediated Fenton-type reactions and that melatonin's highly protective effects against Cr(III) relate, at least in part, to its direct hydroxyl radical scavenging ability.

8-Hydroxy-2'-Deoxyguanosine↗

Changes in lipid peroxidation during pregnancy and after delivery in rats: effect of pinealectomy.

Pregnancy is a physiological state accompanied by a high energy demand of many bodily functions and an increased oxygen requirement. Because of the increased intake and utilization of oxygen, increased levels of oxidative stress would be expected. In the present study, the degree of lipid peroxidation was examined in different tissues from non-pregnant and pregnant rats after the delivery of their young. Melatonin and other indole metabolites are known to be direct free radical scavengers and indirect antioxidants. Thus the effect of pinealectomy at 1 month before pregnancy on the accumulation of lipid damage was investigated in non-pregnant and pregnant rats after the delivery of their young. Malonaldehyde and 4-hydroxyalkenal concentrations were measured in the lung, uterus, liver, brain, kidney, thymus and spleen from intact and pinealectomized pregnant rats soon after birth of their young and at 14 and 21 days after delivery. The same parameters were also evaluated in intact and pinealectomized non-pregnant rats. Shortly after delivery, lipid oxidative damage was increased in lung, uterus, brain, kidney and thymus of the mothers. No differences were detected in liver and spleen. Pinealectomy enhanced this effect in the uterus and lung. It is concluded that during pregnancy high levels of oxidative stress induce an increase in oxidative damage to lipids, which in some cases is inhibited by the antioxidative actions of pineal indoles.

Analysis of Variance↗

Ageing modulates some aspects of the non-specific immune response of murine macrophages and lymphocytes.

The deterioration of the immune system with ageing, which leads to an increased morbidity and mortality from infections, appears to be related to decreases in specific lymphocyte functions. However, the alteration of non-specific immunity is a more controversial subject. Our purpose was to investigate the age-related changes of different functions of the non-specific immune response in peritoneal macrophages (adherence to tissues, mobility directed to a chemical gradient from an infectious focus or chemotaxis, phagocytosis of foreign agents and destruction of these agents by superoxide anion production) and in lymphocytes (adherence and chemotaxis) from peritoneum, axillary lymph nodes, spleen and thymus. We used young (12 weeks), adult (22 weeks), mature (48 weeks) and old (72 weeks) female BALB/c mice. The adherence capacity of macrophages and lymphocytes was greater in adult and old mice than in young animals. The chemotaxis of macrophages showed higher values in cells from young mice than in those from adult mice, increasing again in macrophages from mature and old animals. A similar behaviour was shown by phagocytosis, which reached its highest values in old animals. Anion superoxide production increased with age and again the highest values were obtained in the oldest mice. Conversely, chemotaxis of lymphocytes was higher in the adult and mature animals than in the young and old animals. We conclude that, although there is a decrease in lymphocyte chemotaxis in old animals, the non-specific immune response of macrophages instead of decreasing, may increase in aged mice with respect to the values seen in adult mice.

Aging↗