ascorbic-acid and Lymphoma

Vitamin C is an important micronutrient for various immune cells. It increases phagocytic cell function and is necessary for T and natural killer (NK) cell development. Patients in need of an autologous hematopoietic stem cell transplantation (HSCT) are often vitamin C-depleted. We therefore hypothesized that vitamin C supplementation could improve immune recovery in autologous HSCT patients. This blinded, placebo-controlled trial included 44 patients randomized to receive vitamin C or a placebo. The following outcome measures used were clinical and immunological parameters, among others: time to neutrophil recovery, serum, and intracellular vitamin C values. Twenty-one patients received vitamin C, and 23 received a placebo. The time to neutrophil recovery did not differ between the two groups at 11.2 days (

Topics: Ascorbic Acid; Bacteremia; Hematopoietic Stem Cell Transplantation; Humans; Lymphoma; Multiple Myeloma; Neutrophils; Transplantation, Autologous; Vitamins

Arsenic trioxide (As(2)O(3)) has established clinical activity in acute promyelocytic leukaemia and has pre-clinical data suggesting activity in lymphoid malignancies. Cell death from As(2)O(3) may be the result of oxidative stress. Agents which deplete intracellular glutathione, such as ascorbic acid (AA), may potentiate arsenic-mediated apoptosis. This multi-institution phase II study investigated a novel dosing schedule of As(2)O(3) and AA in patients with relapsed or refractory lymphoid malignancies. Patients received As(2)O(3) 0.25 mg/kg iv and AA 1000 mg iv for five consecutive days during the first week of each cycle followed by twice weekly infusions during weeks 2-6. Cycles were repeated every 8 weeks. The primary end point was objective response. In a subset of patients, sequential levels of intracellular glutathione and measures of Bcl-2 and Bax gene expression were evaluated in peripheral blood mononuclear cells during treatment. Seventeen patients were enrolled between March 2002 and February 2004. The median age was 71, and the majority of enrolled patients had non-Hodgkin's lymphoma (12/17). Sixteen patients were evaluable, and one patient with mantle cell lymphoma achieved an unconfirmed complete response after five cycles of therapy for an overall response rate of 6%. The trial, which had been designed as a two-stage study, was closed after the first stage analysis due to lack of activity. Haematologic toxicities were the most commonly reported events in this heavily pre-treated population, and comprised the majority of grade 3 and 4 toxicities. Intracellular depletion of glutathione was not consistently observed during treatment. As(2)O(3) and AA in this novel dosing strategy was generally well tolerated but had limited activity in patients with relapsed and refractory lymphoid malignancies.

Topics: Adult; Aged; Aged, 80 and over; Arsenic Trioxide; Arsenicals; Ascorbic Acid; Female; Glutathione; Humans; Leukemia; Leukemia, Lymphocytic, Chronic, B-Cell; Lymphoma; Lymphoma, Non-Hodgkin; Male; Middle Aged; Oxides; Safety

We studied erythrocyte and leukocyte superoxide dismutase and catalase activities, erythrocyte malondialdehyde (MDA) and osmotic fragility and plasma L-ascorbic acid and L-dehydroascorbic acid levels in adult patients with acute lymphoblastic leukemia (ALL), Hodgkin's disease (HD) and non-Hodgkin's lymphoma (NHL) before and after treatment. SOD activity was elevated in leukocytes of ALL and HD patients before treatment, and borderlike-significantly elevated in leukocytes of the same patients after treatment in comparison to the control subjects. SOD activity was not changed in NHL patients before or after chemotherapy. Erythrocyte superoxide dismutase and catalase activities were elevated in the three groups of lymphomas before and after treatment. MDA level and osmotic fragility of red blood cells of patients with lymphomas were increased before and after treatment in comparison to the control group. Plasma L-ascorbic acid concentrations were decreased, whereas L-dehydroascorbic acid concentrations were increased in ALL, HD and NHL patients before and after treatment. There were also significant differences in the activities of the antioxidant enzymes, concentrations of antioxidants, MDA and osmotic fragility in the most of the malignant lymphoma patients. The present data suggest that hematological complications and autoimmune hemolytic anemia might be attributed to the oxidative stress produced by malignant lymphomas.

Topics: Adult; Antineoplastic Agents; Antioxidants; Ascorbic Acid; Case-Control Studies; Catalase; Dehydroascorbic Acid; Erythrocyte Membrane; Female; Humans; Leukocytes; Lipid Peroxidation; Lymphoma; Male; Malondialdehyde; Osmotic Fragility; Oxidative Stress; Superoxide Dismutase

Major efforts are underway to identify agents that can potentiate effects of immune checkpoint inhibition. Here, we show that ascorbic acid (AA) treatment caused genomewide demethylation and enhanced expression of endogenous retroviral elements in lymphoma cells. AA also increased 5-hydroxymethylcytosine (5hmC) levels of CD8+ T cells and enhanced their cytotoxic activity in a lymphoma coculture system. High-dose AA treatment synergized with anti-PD1 therapy in a syngeneic lymphoma mouse model, resulting in marked inhibition of tumor growth compared with either agent alone. Analysis of the intratumoral epigenome revealed increased 5hmC with AA treatment, consistent with in vitro findings. Analysis of the tumor immune microenvironment revealed that AA strikingly increased intratumoral infiltration of CD8+ T cells and macrophages, suggesting enhanced tumor immune recognition. The combination treatment markedly enhanced intratumoral infiltration of macrophages and CD8+ T lymphocytes, granzyme B production by cytotoxic cells (cytotoxic T cells and natural killer cells), and interleukin 12 production by antigen-presenting cells compared with single-agent anti-PD1. These data indicate that AA potentiates anti-PD1 checkpoint inhibition through synergistic mechanisms. The study provides compelling rationale for testing combinations of high-dose AA and anti-PD1 agents in patients with aggressive B cell lymphoma as well as in preclinical models of other malignancies.

Topics: 5-Methylcytosine; Animals; Antibodies, Monoclonal; Antineoplastic Agents; Ascorbic Acid; B7-H1 Antigen; CD8-Positive T-Lymphocytes; Cell Line, Tumor; Cell Survival; Combined Modality Therapy; Disease Models, Animal; Drug Synergism; Female; Granzymes; Immunotherapy; Lymphoma; Mice; Mice, Inbred BALB C; Programmed Cell Death 1 Receptor; Tumor Microenvironment

Ascorbyl stearate (Asc-s) is a derivative of ascorbic acid with better anti-tumour efficacy compared to its parent compound ascorbic acid. In this study, we have examined radio-sensitizing effect of Asc-s in murine T cell lymphoma (EL4) cells at 4 Gy. Asc-s and radiation treatment reduced cell proliferation, induced apoptosis in a dose dependent manner by arresting the cells at S/G2-M phase of cell cycle. It also decreased the frequency of cancer stem cells per se, with significantly higher decrease in combination with radiation treatment./Further, Asc-s and radiation treatment increased the level of reactive oxygen species (ROS), drop in mitochondrial membrane potential (MMP) and increased caspase-3 activity resulting in apoptosis of EL4 cells. Further it also significantly decreased GSH/GSSG ratio due to binding of Asc-s with thiols. The increase in oxidative stress induced by Asc-s and radiation treatment was abrogated by thiol antioxidants in EL4 cells. Interestingly, this redox modulation triggered significant increase in protein glutathionylation in a time dependent manner. Asc-s treatment resulted in glutathionylation of IKK, p50-NF-kB and mutated p53, thereby inhibiting cancer progression during oxidative stress. Asc-s quenches GSH ensuing Asc-s + GSH adduct thereby further modulating GSH/GSSG ratio as evident from HPLC and docking studies. The anti-tumour effect of Asc-s along with radiation was studied by injecting EL4 cells in synegenicC57/BL6 male mice. Intraperitoneal injection of Asc-s followed by radiation exposure at 4 Gy to the tumour bearing mice resulted in radio-sensitization which is evident from significant regression of tumour as evident from tumour burden index. The survival study supports the data that Asc-s pre-treatment enhances radio-sensitization in murine lymphoma. Our data, suggest that Asc-s and ionizing radiation induced cell cycle arrest and apoptosis by perturbing redox balance through irreversible complexes of thiols with Asc-s, disturbed mitochondrial membrane permeability and activation of caspase-3 in EL4 cells.

Topics: Animals; Antioxidants; Apoptosis; Ascorbic Acid; Binding Sites; Biomarkers, Tumor; Caspase 3; Cell Cycle Checkpoints; Cell Line, Tumor; Cell Proliferation; Glutathione; Lymphoma; Male; Membrane Potential, Mitochondrial; Mice; Mice, Inbred C57BL; Neoplastic Stem Cells; Oxidative Stress; Radiation, Ionizing; Reactive Oxygen Species; Sulfhydryl Compounds

The aim of the present investigation was to evaluate Zingiber officinale paste against Dalton's lymphoma ascites (DLA)-induced tumours in Swiss albino mice. Experimental animals received Z. officinale paste (low dose 100 mg/kg bw and high dose 500 mg/kg bw) orally for eight alternative days. Treatment with Z. officinale paste showed significant increase in haemoglobin level and decrease in aspartate amino transferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and gamma glutamyl transferase (γ-GT) level. Z. officinale paste reduced the inflammatory mediators and cytokine levels, such as inducible nitric oxide (iNOS), tumour necrosis factor level (TNF-α) and interleukin-1β (IL-1β). Treatment with Z. officinale paste also significantly increased the antioxidant enzyme level, such as superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH) and glutathione transferase (GST), and decreased the lipid peroxidation. Treatment also increased the vitamin C and E levels in treated animals compared with the DLA-bearing host. Histopathological studies also confirmed the protective influence of Z. officinale paste against DLA. The present study suggested that Z. officinale paste could be used as natural spice and a potent antitumour agent.

Topics: Animals; Antioxidants; Ascites; Ascorbic Acid; Biomarkers, Tumor; Cytokines; Gas Chromatography-Mass Spectrometry; Glutathione; Glutathione Transferase; Inflammation Mediators; Liver; Lymphoma; Male; Mice; Plant Extracts; Protective Agents; Zingiber officinale

Chlorambucil is an anticancer drug with alkylating and immunosuppressive activities. Considering various reports on the possible antioxidant/protective functions of ascorbic acid (vitamin C), it was aimed at to explore the modulatory effect of ascorbic acid on therapeutic efficacy and toxicity induced by chlorambucil. Dalton's ascites lymphoma tumor serially maintained in Swiss albino mice were used for the present experiments. The result of antitumor activity showed that combination treatment with ascorbic acid and chlorambucil exhibited enhanced antitumor activity with 170% increase in life span (ILS), which is significantly higher as compared to chlorambucil alone (ILS 140%). Analysis of apoptosis in Dalton's lymphoma tumor cells revealed a significantly higher apoptotic index after combination treatment as compared to chlorambucil alone. Blood hemoglobin content, erythrocytes and leukocytes counts were decreased after chlorambucil treatment, however, overall recovery in these hematological values was noted after combination treatment. Chlorambucil treatment also caused morphological abnormalities in red blood cells, majority of which include acanthocytes, burr and microcystis. Combination treatment of mice with ascorbic acid plus chlorambucil showed less histopathological changes in kidney as compared to chlorambucil treatment alone, thus, ascorbic acid is effective in reducing chlorambucil-induced renal toxicity in the hosts. Based on the results, for further development, hopefully into the clinical usage, the administration of ascorbic acid in combination with chlorambucil may be recommended.

Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Ascites; Ascorbic Acid; Blood Cell Count; Chlorambucil; Hemoglobins; Humans; Lipid Peroxidation; Lymphoma; Mice

Cisplatin treatment caused a significant increase in the life span of ascites Dalton's lymphoma (DL) Tumor-bearing (TB) mice. However, as compared to cisplatin (CP) alone, combination treatment with ascorbic acid plus CP resulted in better therapeutic efficacy against murine DL. Cisplatin treatment of TB mice resulted in the appearance of thickened and irregular arrangement of mitochondrial cristae in the liver, kidney and DL tumor cells. Combination treatment of the hosts with ascorbic acid and CP lessened deformities in the mitochondria of liver and kidney, while in tumor cells, this increased the formation of vacuoles and disruption in mitochondrial cristae. Cisplatin treatment decreased the succinate dehydrogenase (SDH) activity in the mitochondria of kidney and DL cells and combination treatment caused further decrease in SDH activity in kidney and DL cells during 24-48 h of treatment. After CP treatment, the protein content in the mitochondria of these tissues decreased, and during combination treatment, it showed significant improvement. Mitochondrial lipid peroxidation (LPO) increased in these tissues after CP treatment. However, combination treatment significantly decreased mitochondrial LPO in liver and kidney but increased in DL cells. This increase in mitochondrial LPO in DL cells and decrease in liver and kidney could play an important role in the antitumor activity of combination treatment and at the same time reduce CP-induced toxicity in the host. However, further study may be desirable to explore some aspects of the mechanism(s) involved in these changes in mitochondria.

Topics: Animals; Antineoplastic Agents; Antioxidants; Ascites; Ascorbic Acid; Cisplatin; Drug Therapy, Combination; Kidney; Lipid Peroxidation; Lymphoma; Male; Mice; Mitochondria; Mitochondria, Liver; Neoplasms, Experimental; Time Factors

Previous reports from our laboratory have shown that in Swiss female mice exposed to an acute dose (3 Gy) of whole body irradiation (WBI), induced thymic lymphoma (TL) resulted after three to four weeks of exposure. The present study was aimed to further evaluate dependency on gender and effect of age of mice at the time of irradiation on TL incidence. A significant decrease in body weight gain was observed in female mice exposed to WBI, which was found to be correlated with the increase in weight and size of thymus, compared to their respective controls. An increase in TL incidence was observed with the increased postirradiation time, which was 47, 80, and 93% after 90, 120, and 150 days of WBI, respectively, in female mice. In irradiated female mice, the TL incidence was significantly higher and the growth of tumor in terms of weight and size was more aggressive than in males of the same age. Moreover, mice with higher age groups at the time of irradiation showed substantial decrease in TL incidence and its aggressiveness; and these effects were more conspicuous in males than in females. In mice irradiated at the age group of three to four weeks, the TL incidence was 83 and 72% in female and male, respectively, which was decreased to 74% in female and 14% in male in the age group of 12-13 weeks. It was further observed that the postirradiation feeding of animals with antioxidants resulted in a significant decrease in TL incidence, and the prevention in TL incidence was more in animals fed with curcumin (55%) than with ascorbic acid and eugenol (20%). These results have provided significant new findings on the phenomenon of radiation-induced TL incidence related to gender and age at the time of irradiation and its prevention by postirradiation antioxidant feeding to mice.

Topics: Aging; Animals; Antioxidants; Ascorbic Acid; Body Weight; Curcumin; Eugenol; Female; Gamma Rays; Lymphoma; Male; Mice; Neoplasms, Radiation-Induced; Organ Size; Sex Factors; Thymus Gland; Thymus Neoplasms; Whole-Body Irradiation

Human pharmacokinetics data indicate that i.v. ascorbic acid (ascorbate) in pharmacologic concentrations could have an unanticipated role in cancer treatment. Our goals here were to test whether ascorbate killed cancer cells selectively, and if so, to determine mechanisms, using clinically relevant conditions. Cell death in 10 cancer and 4 normal cell types was measured by using 1-h exposures. Normal cells were unaffected by 20 mM ascorbate, whereas 5 cancer lines had EC(50) values of <4 mM, a concentration easily achievable i.v. Human lymphoma cells were studied in detail because of their sensitivity to ascorbate (EC(50) of 0.5 mM) and suitability for addressing mechanisms. Extracellular but not intracellular ascorbate mediated cell death, which occurred by apoptosis and pyknosis/necrosis. Cell death was independent of metal chelators and absolutely dependent on H(2)O(2) formation. Cell death from H(2)O(2) added to cells was identical to that found when H(2)O(2) was generated by ascorbate treatment. H(2)O(2) generation was dependent on ascorbate concentration, incubation time, and the presence of 0.5-10% serum, and displayed a linear relationship with ascorbate radical formation. Although ascorbate addition to medium generated H(2)O(2), ascorbate addition to blood generated no detectable H(2)O(2) and only trace detectable ascorbate radical. Taken together, these data indicate that ascorbate at concentrations achieved only by i.v. administration may be a pro-drug for formation of H(2)O(2), and that blood can be a delivery system of the pro-drug to tissues. These findings give plausibility to i.v. ascorbic acid in cancer treatment, and have unexpected implications for treatment of infections where H(2)O(2) may be beneficial.

Topics: Antioxidants; Apoptosis; Ascorbic Acid; Cell Line, Tumor; Dose-Response Relationship, Drug; Free Radicals; Humans; Hydrogen Peroxide; Lymphoma; Oxidation-Reduction; Prodrugs

Oral treatment with 50 mg X kg(-1) day(-1) of crude methanol extract of Centella asiatica for 14 days significantly increased the anti-oxidant enzymes, like superoxide dismutase (SOD), catalase and glutathione peroxidase (GSHPx), and anti-oxidants like glutathione (GSH) and ascorbic acid decreased in lymphoma-bearing mice.

Topics: Administration, Oral; Animals; Antioxidants; Ascorbic Acid; Catalase; Centella; Glutathione; Glutathione Peroxidase; Kidney; Liver; Lymphoma; Male; Mice; Phytotherapy; Plant Extracts; Superoxide Dismutase

Apurinic/apyrimidinic endonuclease is a key enzyme in the process of base excision repair, required for the repair of spontaneous base damage that arises as a result of oxidative damage to DNA. In mice, this endonuclease is coded by the Apex gene, disruption of which is incompatible with embryonic life. Here we confirm the embryonic lethality of Apex-null mice and report the phenotypic characterization of mice that are heterozygous mutants for the Apex gene (Apex+/-). We show that Apex heterozygous mutant cells and animals are abnormally sensitive to increased oxidative stress. Additionally, such animals manifest elevated levels of oxidative stress markers in serum, and we show that dietary supplementation with antioxidants restores these to normal levels. Apex+/- embryos and pups manifest reduced survival that can also be partially rescued by dietary supplementation with antioxidants. These results are consistent with a proposed role for this enzyme in protection against the deleterious effects of oxidative stress and raise the possibility that humans with heterozygous mutations in the homologous HAP1 gene may be at increased risk for the phenotypic consequences of oxidative stress in cells.

Topics: Adenocarcinoma, Papillary; Animals; Ascorbic Acid; Carbon-Oxygen Lyases; Cell Survival; Cells, Cultured; Dietary Supplements; Dinoprost; DNA-(Apurinic or Apyrimidinic Site) Lyase; Dose-Response Relationship, Drug; Embryo, Mammalian; Female; Fibroblasts; Genotype; Heterozygote; Lipid Peroxides; Lung Neoplasms; Lymphoma; Male; Mice; Mice, Inbred C57BL; Mice, Inbred Strains; Mice, Mutant Strains; Oxidative Stress; Paraquat; Phenotype; Vitamin E; Vitamin K

Arsenic trioxide (As2O3) induces clinical remission in acute promyelocytic leukemia (APL) with minimal toxicity and apoptosis in APL-derived NB4 cells at low (1 to 2 micromol/L) concentration. We examined the basis for NB4 cell sensitivity to As2O3 to identify experimental conditions that would render other malignant cells responsive to low concentrations of As2O3. The intracellular glutathione (GSH) content had a decisive effect on As2O3-induced apoptosis. Highly sensitive NB4 cells had the lowest GSH and the sensitivity of other cell lines was inversely proportional to their GSH content. The t(14;18) B-cell lymphoma cell line had low GSH levels and sensitivity to As2O3 at levels slightly higher than in APL cells. Experimental upmodulation of GSH content decreased the sensitivity to As2O3. Ascorbic acid and buthionine sulfoxide (BSO) decreased GSH to a greater extent, and rendered malignant cells more sensitive to As2O3. As2O3-induced apoptosis was not enhanced by ascorbic acid in normal cells, suggesting that the combination of ascorbic acid and As2O3 may be selectively toxic to some malignant cells. Ascorbic acid enhanced the antilymphoma effect of As2O3 in vivo without additional toxicity. Thus, As2O3 alone or administered with ascorbic acid may provide a novel therapy for lymphoma.

Topics: Acetylcysteine; Animals; Antineoplastic Agents; Apoptosis; Arsenic Trioxide; Arsenicals; Ascorbic Acid; Cells, Cultured; Drug Synergism; Glutathione; Growth Inhibitors; Hematopoietic Stem Cells; HL-60 Cells; Humans; Lymphoma; Mice; Mice, Inbred Strains; Oxidation-Reduction; Oxides; Tumor Cells, Cultured

Combined effects of ascorbic acid (vitamin C) and cisplatin on the growth of Dalton's lymphoma in C3H/He mice was investigated. Chemotherapy with sub-therapeutical dose (3 mg/kg) enabled to increase the survival time of the tumor bearing mice without any tumor free survivors. Ascorbic acid enhances the antitumor effect of cisplatin in vivo resulting in 60/70 day survivors along with tumor free survivors. Ascorbic acid also enhances the efficacy of low dose of cisplatin (5 micrograms/ml) in vitro. Tumor cells incubated with cisplatin and ascorbic acid, when injected into normal mice, exhibited inhibited growth resulting in an increased life span of tumor bearing mice and tumor free survivors. Inoculation of tumor cells incubated with cisplatin (5 micrograms/ml) and different concentrations (25 or 50 micrograms/ml) of ascorbic acid resulted in 30% tumor free mice which was not observed when concentration of cisplatin increased to 10 micrograms/ml in the medium. A possible cause of the enhancement of cisplatin-induced tumor growth inhibition may be the modulation of permeability of tumor cell membrane by ascorbic acid which increases the uptake of cisplatin into tumor cells, making less efficient the DNA repair machinery due to increased efficiency of adduct formation in DNA molecule. Possibly, this effect of ascorbic acid renders cisplatin more effective as an antitumor agent.

Topics: Animals; Antineoplastic Combined Chemotherapy Protocols; Ascorbic Acid; Cell Division; Cisplatin; Combined Modality Therapy; Dose-Response Relationship, Drug; Drug Synergism; Female; Immunotherapy; Lymphoma; Male; Mice; Mice, Inbred C3H; Neoplasm Transplantation; Tumor Cells, Cultured

The influence of external abdominal irradiation and cytostatic therapy on the vitamin status was studied in patients with cancer of the uterus, bladder or prostate and in patients with malignant lymphoma. It was found that the vitamin status of these patients at the beginning of therapy in general was adequate, though vitamin A and vitamin D levels were reduced. During radiotherapy decreases of vitamin E, vitamin C, vitamin B12 and folic acid levels were observed. Chemotherapy caused a decrease of the folic acid levels after a few months. No clinical symptoms of vitamin deficiency were observed.

Topics: Ascorbic Acid; Calcifediol; Female; Humans; Lymphoma; Male; Neoplasms; Prostatic Neoplasms; Urinary Bladder Neoplasms; Uterine Neoplasms; Vitamin A; Vitamin B 12; Vitamin E; Vitamins

Both sodium ascorbate and ascorbic acid were tested at millimolar concentrations in the mouse lymphoma L5178Y TK+/- cell for chemically-induced cytotoxicity and the induction of gene mutations at the thymidine kinase locus as detected by increased trifluorothymidine-resistance. Neither chemical caused any dose-related increases in trifluorothymidine resistance, even at toxic levels. Increased hydrogen ion concentration was not itself a contributing factor to ascorbic acid toxicity. Ascorbate toxicity was due to products formed in vitro in the absence of cells via chemical reactions with medium components. The formation or persistence of these toxic substances could be prevented by co-incubation with catalase prior to the addition of L5178Y cells. These results suggest that ascorbic acid would not be a mammalian cell mutagen normal physiological conditions.

Topics: Animals; Ascorbic Acid; Cell Line; Cell Survival; Culture Media; Dose-Response Relationship, Drug; Lymphoma; Mice; Mutagenicity Tests; Mutagens; Mutation; Neoplasms, Experimental; Sodium; Thymidine Kinase

Topics: Adolescent; Adult; Aged; Anemia; Ascorbic Acid; Child, Preschool; Deferoxamine; Drug Therapy, Combination; Female; Humans; Iron; Liver Diseases; Lymphoma; Male; Middle Aged

Topics: Agglutination Tests; Ascorbic Acid; Candida; Candidiasis; Humans; Immunodiffusion; In Vitro Techniques; Iron; Leukemia, Lymphoid; Leukemia, Myeloid; Leukemia, Myeloid, Acute; Lymphoma; Multiple Myeloma; Polycythemia Vera; Precipitin Tests; Transferrin

Topics: Animals; Ascorbic Acid; Carcinoma, Ehrlich Tumor; Carcinoma, Hepatocellular; Liver; Liver Neoplasms; Lymphoma; Lymphoma, Non-Hodgkin; Metabolism; Mice; Microsomes; Microsomes, Liver; Neoplasms; Neoplasms, Experimental; Oxidoreductases; Research

Topics: Adrenal Glands; Adrenocorticotropic Hormone; Ascorbic Acid; Histamine; Lymphoma; Lymphoma, Non-Hodgkin; Sarcoma; Vitamins