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At least 775 records · Page 43Linked to original sources
PubMed1983

Rapid characterization of cellular retinoid-binding proteins by high-performance size-exclusion chromatography.

A high-performance size-exclusion chromatographic method was developed for the analysis of cellular retinol and retinoic acid-binding proteins. The chromatographic analysis of the retinol-retinol-binding protein complex or the retinoic acid-retinoic acid-binding protein complex requires 15 min. The use of high-specific-radioactivity retinoid ligand (30-40 Ci/mmol) allows routine detection of 25 fmol of retinoid-binding protein/mg of cytosolic protein. Thus, this method provides a rapid alternative to sucrose density gradient sedimentation analysis of the cellular retinoid-binding proteins. High-performance size-exclusion chromatography is well suited to screening novel tissues, tumors, and cell lines for the presence of retinoid-binding proteins and to the further characterization of these cellular proteins. This method was applied to the characterization of cellular retinol- and retinoic acid-binding proteins in fetal rabbit tissues. Both retinol- and retinoic acid-binding proteins were detected in fetal rabbit brain, intestine, kidney, and lung at a gestational age of 28 days. Neither retinoid-binding protein was detected in 28-day-old fetal rabbit placenta. Specific retinoic acid binding in fetal intestinal cytosol decreased as a function of increasing gestational age.

Animals↗
PubMed1994

Spatial distribution of endogenous retinoids in the murine embryonic mandible.

Retinoids play an important part in pattern formation during embryonic development. Exogenous retinoids alter the pattern of skeletal, neural and odontogenic tissues. Endogenous retinoids have been demonstrated previously in the murine embryonic mandible, reaching a concentration peak during the initiation of odontogenesis. It was now found that endogenous retinoids are present in a concentration gradient in the embryonic mouse mandible at the time of the initiation of the dental lamina. All-trans-retinoic acid was more concentrated in the incisor region and retinol in the molar region. These results, and the fact that exogenous retinoids produce supernumerary incisors and missing molars, suggest that all-trans-retinoic acid may instruct incisor morphology.

Animals↗
PubMed1991

Effect of light on endogenous ligands carried by interphotoreceptor retinoid-binding protein.

Interphotoreceptor retinoid-binding protein (IRBP) is a vitamin A carrier present only in the extracellular material lying between the neural retina and the retinal pigment epithelium of vertebrate eyes. The amount of retinol bound endogenously by IRBP in this interphotoreceptor space is known to increase upon illumination. This finding led to the hypothesis that IRBP may act as a shuttle for vitamin A during the visual cycle that regenerates rhodopsin. In the present work, we separated IRBP from other retinoid-binding proteins in bovine interphotoreceptor matrix preparations by means of size-exclusion chromatography. IRBP's endogenous ligands were retained during this procedure and were then extracted into hexane and analysed by normal-phase HPCL. We found that IRBP carries, in a light-dependent manner, all the retinoid isomers involved in the visual cycle. For dark-adapted eyes the amounts of bound ligands are (in nmol per eye) 0.09 all-trans retinol, 0.11 11-cis retinol, 0.04 all-trans retinal, 0.16 11-cis retinal, and 0.07 retinyl esters. For light-adapted eyes the amount of all-trans retinol was found to increase by a factor of five, and that of 11-cis retinal to decrease by a factor of four. (These eyes contain 3.1 nmol of IRBP, which does not change in amount with lighting conditions). Thus, the major endogenous ligand of IRBP is 11-cis retinaldehyde in the dark and all-trans retinol in the light. The data are consistent with a role for IRBP as a non-selective scavenger and stabilizer of retinoids released from photoreceptors and pigment epithelial cells. However, it cannot be concluded from these data that IRBP is involved in directed transport of retinoids across the interphotoreceptor matrix, since there is no evidence for the appropriate spatial gradients in the ligands bound to the protein.

Adaptation, Ocular↗
PubMed1985

Time and dose responses of the reduction in retinoid concentrations in C57BL/Rij and DBA/2 mice induced by 3,4,3',4'-tetrachlorobiphenyl.

A single ip dose of 15 mg 3,4,3',4'-tetrachlorobiphenyl (TCB)/kg induced a 30 to 40% reduction of retinol and retinyl palmitate concentrations in hepatic tissue of C57BL/Rij mice within 2 to 4 days. This level of reduction was maintained for about 14 days. The ED50 was 32 mg TCB/kg for hepatic retinol and 17 mg TCB/kg for hepatic retinyl palmitate. In DBA/2 mice, however, no reduction in hepatic retinoids was observed even at doses up to 729 mg TCB/kg. The duration of the reduction in hepatic retinoids did not correlate with the induced aryl hydrocarbon hydroxylase (AHH) activity in C57BL/Rij mice. These data suggest that AHH and related enzymes are not directly involved in the TCB-induced reduction in retinoids in these mouse strains. No significant differences in the accumulation of TCB in hepatic tissues of C57BL/Rij and DBA/2 mice were observed; however, the estimated elimination rate in C57BL/Rij was two times faster than that in DBA/2 mice. In serum of DBA/2 mice, a rapid 50% decline in the concentration of retinol was observed after only 2 to 6 hr, remaining at the reduced value for about 14 days. The ED50 for serum retinol was 1 to 2 mg TCB/kg. Only a transient reduction in serum retinol, disappearing within 48 hr, was observed in the C57BL/Rij mouse. TCB accumulated to an almost 15-fold higher extent in serum of DBA/2 mice as compared with C57BL/Rij mice. The effect of TCB on retinoids in a few other strains of mice and in the Sprague-Dawley rat showed a reduction in serum retinol rather than in hepatic retinoids.

Animals↗
PubMed1989

Retinoid-induced hemorrhaging and bone toxicity in rats fed diets deficient in vitamin K.

The recent increase in the clinical use of synthetic vitamin A compounds has led to concern of possible side effects. Some of these effects are known to be influenced by dietary levels of vitamin K. We therefore compared the toxic effects of 13-cis-retinoic acid (13cisRA), retinyl acetate (ROAc), and N-(4-hydroxyphenyl)retinamide (4HPR) in male Sprague-Dawley rats maintained on diets containing different levels of vitamin K. Animals were fed either an NIH-07 diet supplemented with menadione (3.1 ppm vitamin K3), an NIH-07 diet not supplemented with menadione, or an AIN-076 purified diet devoid of vitamin K. The retinoids had no effect on prothrombin times of animals fed the supplemented diet. When menadione was omitted from the diet, however, 4HPR-dosed animals had elevated prothrombin times. This effect was observed as early as Day 7 and was accompanied by one confirmed hemorrhagic death. 13cisRA-dosed animals showed no change in prothrombin times. In the high-dose ROAc group, there was a twofold increase in prothrombin times but only after prolonged dosing. In animals fed the NIH-07 diets, 13cisRA and ROAc induced multiple bone fractures at all dose levels. In contrast, 4HPR administered at the highest dose induced only one fracture in one animal. Animals fed the purified diet lost weight faster and diet sooner than those maintained on the other diets. Bone fractures were not observed in these animals because of early deaths resulting from hemorrhaging. For all retinoid-dosed groups maintained on the purified diet, changes in prothrombin times occured as early as 1 week. The order of effect was 4HPR greater than ROAc greater than 13cisRA, with increases in prothrombin times correlating with increases in hemorrhagic deaths. Hence, the degree of retinoid-induced hemorrhage, but not the incidence of bone fractures, was inversely related to vitamin K levels in the diet. 13cisRA and ROAc, but not 4HPR, caused a dose-dependent reduction in plasma osteocalcin, an effect that correlated with retinoid-induced bone effects. In contrast, serum alkaline phosphatase was elevated in animals dosed with 13cisRA or 4HPR but not in those dose with ROAc. For this enzyme, the electrophoretic pattern on agarose gel showed a decrease, compared to controls, in the major isozyme in serum of ROAc-dosed animals. Hence, plasma osteocalcin is a better predictor of retinoid-induced bone effects than serum alkaline phosphatase.

Alkaline Phosphatase↗
PubMed1984

Interphotoreceptor retinoid-binding protein. Characteristics in bovine and monkey retina.

Evidence is presented for the presence of a unique retinoid-binding protein in the retinal interphotoreceptor space (IPS). The protein is a glycoprotein with an apparent native Mr of approx. 250,000 and subunit Mr of about 146,000. It is synthesized by the retina and appears to be quickly secreted into the IPS. The protein binds retinol endogenously and there is an apparent differential light-dark binding of the ligand. The protein will bind other retinoids as well as retinol and thus is not as ligand specific as is the cellular retinol-binding protein (CRBP). With the localization of this protein in the IPS and its relatively catholic taste in retinoid binding, it is reasonable to call it the interphotoreceptor retinoid-binding protein (IRBP). The protein may function as a retinoid transport vehicle between retina and pigment epithelium.

Animals↗
PubMed1989

Retinoids as potential chemopreventive agents in squamous cell carcinoma of the head and neck.

Although newer combined modality approaches, including neoadjuvant cytotoxic chemotherapy, for patients with squamous cell carcinoma (SCCA) of the head and neck have produced high initial complete response rates, they have not improved overall survival for patients with advanced disease. Vitamin A plays an essential role in the normal differentiation of epithelial tissues. Retinoids, analogs of vitamin A, are active in certain premalignant and malignant disorders including SCCA. Six studies, including one recently reported placebo-controlled randomized trial, have demonstrated the efficacy of retinoids in oral leukoplakia. Two studies (totalling 48 patients) have shown significant retinoid activity (67% overall complete response rate) in patients with aggressive, recurrent laryngeal papillomatosis. Two trials (including a randomized phase II trial) of isotretinoin in advanced, refractory SCCA of the head and neck have produced an objective response rate of 16%, which is comparable to that reported in single-agent studies with cytotoxic drugs. There is a need for further study of retinoids in head and neck cancer. The high initial response rates with current therapy and the high subsequent risks of local recurrence and of developing second primary tumors in head and neck cancer patients offer an excellent opportunity to investigate the use of retinoids as adjuvant therapy for this malignancy.

Carcinoma, Squamous Cell↗
PubMed1989

Retinoid binding proteins and human skin.

New techniques for the analysis of proteins with specific binding for natural retinoids in human plasma and skin extracts have been developed. Polyacrylamide gel electrophoresis (PAGE), followed by protein blotting with an antiserum specific to retinol-binding protein (RBP), the plasma carrier of retinol, showed that: (1) retinoic acid induced striking conformational changes when bound to RBP, and (2) none of the several synthetic retinoids used in human therapy were found to bind to RBP. This directly confirms and extends previous indirect observations that synthetic retinoids are not delivered to the target organs through RBP. Human skin extracts incubated with either [3H]retinol or [3H]retinoic acid and analyzed by PAGE is a novel technique for the study of cellular retinol-(CRBP) and retinoic acid-(CRABP) binding proteins; it allows one to more specifically analyse these binding proteins and differentiate them from RBP. This technique confirmed and extended our previous observations: (1) CRABP is present in much higher amounts in the epidermis than in the dermis, whereas CRBP is detectable in very low amounts in both tissues, (2) a dramatic increase of CRABP is found in psoriatic plaques and (3) there is an up-modulation of epidermal CRABP during systemic or topical synthetic retinoid therapy. When the ability of some synthetic analogs of retinoic acid to compete with [3H]retinoic acid binding on human skin CRABP was studied, two important observations were made: (1) the analogs that, when given to human subjects were pharmacologically active, were found to be good competitors and vice-versa, (2) no strict correlation was found between the IC50 and the pharmacological potency of the retinoid.

Biological Transport↗
PubMed1986

Synthesis of cellular and extracellular glycoproteins by cultured human keratinocytes and their response to retinoids.

The glycoproteins synthesized by human keratinocytes cultured on 3T3 feeder layers were studied by metabolic labelling. Keratinocytes freed of feeder cells synthesized a complex pattern of cellular and extracellular glycoproteins that was distinct from that of 3T3 cells, dermal fibroblasts and epidermal melanocytes. The effect of low concentrations of all-trans-retinoic acid and arotinoid ethyl ester on glycoprotein synthesis was examined in keratinocyte cultures depleted of vitamin A. Treatment with either retinoid resulted in a 2-3-fold increase in the amount of D-[3H]glucosamine-labelled material in the culture medium. Gel electrophoresis revealed increased incorporation of D-[3H]glucosamine into extracellular glycoproteins of Mr 245,000, 170,000, 140,000, 130,000, 120,000 and 105,000 as well as into glycosaminoglycans in retinoid-treated cultures. The labelling of extracellular glycoproteins with L-[3H]leucine and L-[35S]methionine was also increased by retinoids suggesting increased synthesis of these components rather than an effect on their glycosylation. The Mr 245 000 glycoprotein was identified as keratinocyte-derived fibronectin by immunoblotting, immunoprecipitation and specific binding to gelatin. The results show that retinoids increase the synthesis of glycoprotein as well as glycosaminoglycan components of the extracellular matrix in human keratinocyte cultures. It is suggested that retinoids select for a population of cells that synthesize relatively large amounts of glycosaminoglycan, fibronectin and other as yet unidentified extracellular glycoproteins.

Benzoates↗
PubMed1991

Potentiation of retinoid-induced differentiation of HL-60 and U937 cell lines by cytokines.

Retinoids varied in their capacity to induce differentiation in HL-60 cells in this order: Ro 13-6307, tretinoin, isotretinoin, acitretin and Ro 13-7410 (high to low). In contrast, retinoids lacking a polar carboxylic acid, such as temarotene and Ro 14-6113, were inactive. Various cytokines had no differentiation-inducing effect by themselves. However, the addition of cytokines to retinoids increased differentiation. Combined with tretinoin, cytokines increased differentiation in this order: interferon (IFN) gamma, granulocyte colony-stimulating factor, interleukin-1 alpha (IL-1 alpha), IL-4, tumour necrosis factor alpha and IFN-alpha. Combination of cytokines with isotretinoin, acitretin, Ro 13-7410, and Ro 13-6307 showed a similar pattern of potentiation to that of tretinoin. Temarotene or Ro 14-6113 did not induce differentiation, alone or with cytokines. Combinations of cytokines were not synergistic in the presence of retinoids; antagonism was even observed. In U937 cells, lower levels of differentiation-induction were observed. Potentiation of the differentiation-inducing effect of retinoids by cytokines might indicate a clinical differentiation therapy of tumours.

Cell Differentiation↗
PubMed1989

Marked alterations in retinoid homeostasis of Sprague-Dawley rats induced by a single i.p. dose of 10 micrograms/kg of 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Interference of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in retinoid homeostasis was investigated in Sprague-Dawley rats with a low (dietary induced) retinoid status, that were fed a [3H]retinol-containing diet (37 MBq, 10,000 IU/kg diet) for 21 days to facilitate determination of retinoid concentrations in various tissues. The rats were exposed to a single i.p. dose of 10 micrograms TCDD/kg body weight in corn oil, or to corn oil at day 7 of [3H]retinol supplementation. TCDD induced significant reductions in retinol and retinyl ester concentrations and [3H] retinol-derived radioactivity in the liver, the lung, the intestine and the adrenals to 3-5%, 40-45%, 37%, and 56% of control values, respectively, at 14 days after exposure. In contrast, the retinoid concentrations and the amount of [3H]retinol-derived radioactivity in the kidney and serum of TCDD-treated rats was increased to 440% and 140% of corn oil-treated controls, respectively, at the termination time of the experiment. Analysis of the amount of serum retinol binding protein (RBP) by gel-permeation chromatography revealed an 150% increase in the free fraction of retinol-RBP, i.e., uncoupled to transthyretin (TTR), in serum of TCDD-treated rats. In addition, urinary excretion of [3H]retinol-derived radioactivity was significantly enhanced (to 140% of controls) by TCDD. These data indicate that TCDD induces an increased mobilization of retinoids from hepatic and extrahepatic storage sites into serum accompanied by an enhanced elimination via the kidney into the urine of rats.

Adrenal Glands↗
PubMed1993

Improving medical approaches to primary CNS malignancies--retinoid therapy and more.

Successfully inducing differentiation in ectodermal diseases, retinoids harbour considerable therapeutic potential in the treatment of neuroectodermal-neuroepithelial malignancies. The principal tissue retinoid, retinoic acid, can be potently upregulated in vivo by a relatively specific catabolic inhibitor, R75251 (liarozole). Both substances have been given orally over 2 years in addition to standard treatment, and have been well tolerated. Corresponding closely to plasma retinoid levels, cutaneous side effects facilitate individual dosing. We evaluate this adjuvant retinoid approach and additional efforts to improve therapy of primary CNS malignancies, including the topical administration of retinoids in gamma linolenic acid.

Aged↗
PubMed1992

Effects of retinoids on endothelial cell proliferation, prostacyclin production and platelet aggregation.

In addition to their anti-inflammatory and anti-cancer activities, retinoids have been shown to affect angiogenesis, endothelial proliferation and the process of wound healing. While peripheral vascular occlusion has not been observed as an adverse effect clinically, the effects of retinoids on prostacyclin production in endothelial cells and platelet aggregation are not known. We examined the effects of tretinoin, isotretinoin and etretinate (3.3 x 10(-8) to 3.3 x 10(-5) M) on cytotoxicity by 51Cr-release assay, growth and prostacyclin in bovine carotid endothelial cell cultures, and the aggregation of human platelets induced by ADP. All retinoids showed either no or only small effects on cytotoxicity and human platelet aggregation. Prostacyclin production was not significantly affected except for tretinoin and isotretinoin at 3.3 x 10(-5) M. Endothelial proliferation was affected by all three retinoids in a dose-dependent fashion; for tretinoin and isotretinoin an inhibitory trend was noted as the concentration increased but the reverse was true for etretinate. Retinoids at 3.3 x 10(-5) M induced alterations of typical endothelial morphology; the cells became fibroblastoid. The results of prostacyclin production and platelet aggregation in the present study are consistent with the absence of peripheral vascular occlusion as a side effect clinically.

Animals↗
PubMed2005

Surgical stress-induced alterations in retinoid metabolism in the small intestine: role of oxygen free radicals.

Oxidative stress in the small intestine can result in altered cell proliferation, migration, and differentiation of villus-crypt cells. Retinoid metabolism is recognized as an important mediator of cellular differentiation in the intestine. This study examined the effect of oxidative stress in retinoid metabolism in a surgical stress model. Surgical stress was performed by handling the intestine as done during laparotomy. Villus-crypt cells were isolated at different time periods and various retinoid concentrations in the cell homogenate and the retinoic acid forming enzymes were quantitated using HPLC. Surgical stress resulted in altered retinoid levels in various cell populations in the small intestine at 1 and 12h. The activity of alkaline phosphatase and retinal oxidase was also altered at these time points and all these changes were prevented by inhibiting superoxide generation using xanthine oxidase inhibitor, allopurinol. These studies suggest that alterations seen in enterocytes during surgical stress may be mediated by changes in retinoid metabolism.

Aldehyde Oxidoreductases↗
PubMed2005

Retinoid metabolism during development of liver cirrhosis.

The changes in retinoid metabolism have been documented in liver cirrhosis. However, the dynamic alterations in levels of this vitamin between circulation and liver during development of the liver cirrhosis are not well understood. The aim of this study was to measure retinoids in the liver and circulation in parallel, during and after development of cirrhosis induced by carbon tetrachloride and thioacetamide. Retinoid levels were measured by HPLC. A decrease in retinaldehyde and total retinol, together with an increase in retinoic acid was evident in liver from both carbon tetrachloride or thioacetamide treated rats within a month after initiation of treatment. Activity of enzymes involved in retinoid metabolism such as retinaldehyde oxidase, retinaldehyde dehydrogenase, and retinaldehyde reductase were decreased in the liver. In parallel, levels of retinol and retinaldehyde in the serum were increased while retinoic acid was decreased. This study indicates that during development of cirrhosis, there is reciprocal transfer of retinoid metabolites between the circulation and the liver.

Aging↗
PubMed2005

Cancer prevention by retinoids and carotenoids: independent action on a common target.

Virtually all human tumors are deficient in gap junctional communication (GJC) and the restoration of GJC by forced expression of connexins reduces indices of neoplasia. The expression of connexin 43 (Cx43) is upregulated by cancer-preventive retinoids and carotenoids which correlates with the suppression of carcinogen-induced transformation in 10T1/2 cells. However, the molecular mechanism for upregulated expression is poorly understood. The retinoic acid receptor antagonist, Ro 41-5253, suppressed retinoid-induced Cx43 protein expression in 10T1/2 cells and the induction of a Cx43 luciferase reporter construct in F9 cells, but did not suppress protein expression or reporter activity induced by the non-pro-vitamin A carotenoid astaxanthin. In contrast, Cx43 induction by astaxanthin, but not by a RAR-specific retinoid, was inhibited by GW9662, a PPAR-gamma antagonist. Neither compound required protein synthesis for the induction of Cx43 mRNA, nor was the 5.0 h half-life of Cx43 mRNA altered, indicating direct transcriptional activation. The responsive region was found within -158 bp and +209 bp of the transcription start site. Site directed mutagenesis of a GC-box in this region increased basal levels of transcription and loss of retinoid responsiveness. Simultaneous treatment with a retinoid and beta-carotene or astaxanthin resulted in supra-additive Cx43 expression, again indicating separate mechanisms of gene regulation.

Animals↗
PubMed2005

Topical retinoids in inflammatory acne: a retrospective, investigator-blinded, vehicle-controlled, photographic assessment.

BACKGROUND: Despite published data showing the efficacy of topical retinoids in treating inflammatory acne, in clinical practice topical retinoids tend to be used most commonly for noninflammatory acne. OBJECTIVE: The goal of this study was to assess the efficacy of topical retinoids as monotherapy in inflammatory acne. METHODS: This retrospective, investigator-blinded,vehicle-controlled, photographic assessment study was conducted by 5 investigators. The investigators rated pretreatment and posttreatment photographs of patients who had participated in 12- or 15-week, double-blind comparisons of tazarotene 0.1% gel, adapalene 0.1% gel, tretinoin 0.1% microsponge, tretinoin 0.025% gel, and tazarotene 0.1% cream (vehicle). Acne severity was rated on a 7-point scale. A posttreatment increase or decrease of 1 grade was considered clinically meaningful; > or =2 grades was considered an even clearer measure of clinically significant improvement. Investigators also rated global response to treatment on a 7-point scale. A posttreatment increase of > or =2 grades was considered a clinically relevant improvement. RESULTS: Each of the 5 investigators rated photographs of 577 patients ( approximately 52% women, approximately 48% men; mean age, 18-20 years), for a total of 2885 evaluations (in addition to daily evaluations of the 20 control patients). The treatment groups consisted of tazarotene (252 patients, 1260 evaluations), adapalene (178 patients, 890 evaluations), tretinoin microsponge (47 patients, 235 evaluations), tretinoin gel (39 patients, 195 evaluations), and vehicle (61 patients, 305 evaluations). Inflammatory acne was improved with all 4 retinoids compared with vehicle. In 1905 evaluations in which pretreatment acne severity was grade > or =3 (mild to moderate), the incidences of clinically significant improvements in the tazarotene, adapalene, and tretinoin microsponge groups were 24%, 17%, and 21%, respectively (all, P < or = 0.001 vs vehicle [7%]). The difference in prevalence of clinically significant improvement was statistically similar between the tretinoin gel and vehicle groups. The incidences of clinically relevant improvement in global response to tazarotene, adapalene, tretinoin microsponge, and tretinoin gel were 36%, 34%, 31%, and 28%, respectively (P < or = 0.001, < or =0.001, < or =0.001, and < or =0.01, respectively, vs vehicle [17%]). CONCLUSIONS: : The results of this study suggest that topical retinoid monotherapy can achieve clinically significant improvements in inflammatory acne.

Acne Vulgaris↗
PubMed2003

Automated solid-phase extraction and liquid chromatographic method for retinoid determination in biological samples.

In this study, a method for partly automated sample preparation and fully automated solid-phase extraction method for plasma, kidney and liver samples for various retinoids like all-trans-4-oxo-retinoic acid, 13-cis-4-oxo-retinoic acid, 13-cis-retinoic acid, 9-cis-retinoic acid, all-trans-retinoic acid, retinol and retinyl palmitate was established. Plasma, embryo-, kidney-and liver-homogenates were automatically mixed and extracted on multiple usage solid-phase (C2) extraction cartridges immediately before HPLC analysis. Automated cleaning, preconditioning and incorporation of the loaded cartridge to fully automated HPLC separation and quantification of the various retinoids in a single HPLC run was established. The recovery of the retinoids was generally between 80 and 90%. Intra-day repeatability was < 11.7%. As little as 1.2 ng/ml could be quantified in lipid-mixture standard samples. This method allows a highly automated sample preparation and a fully automated solid-phase extraction with good selectivity for the study of endogenous retinoids and retinoids after nutritional supplementations and pharmacological applications in several biological samples.

Animals↗