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Below is a letter supporting the use of antioxidants during chemotherapy with supportive medical literature. 
 
Claiming to treat something like cancer is a bit like claiming to treat something like colds, except in this case we have a different cold specialist for each eye, each ear, and every part of the nostril.  Oncologists will rightly yell that I have little to no experience with your particular subsection of cancer and that might be correct.  But my reply is that despite all the extensive specialization we have been unable to stem the tide of cancer.  Perhaps a slightly wider view of the whole body system would be beneficial. 
 
With every cancer patient I dedicate myself to learning the most up-to-date standard treatments as well as the alternative treatments for the standard treatment side effects. 
 
I generally co-treat alongside oncologists, with varying levels of tolerance on their part.  In most cases I must say that I have received the best communication from the highest ranked specialists in the Boston area so I tend to refer patients that far south.  I have also received some excellent cooperation from Portland specialists.  My experience locally has been less of a cooperative venture, as I think the letter below attests: 
 

Information provided to prospective patient told to avoid antioxidants by her oncologist locally. 

 

Summary:  In the discussion of antioxidants and chemotherapy, the information available (Hodgkins Lymphoma specifically and more generally) does not support avoidance.  Preliminary data support either no effect or, more concerning, a possible causative link between low antioxidant levels and the proliferation of lymphoma.  Given the information available, advice to avoid antioxidants must be based on clinical evidence from medical research.  This author was unable to find any research other than an anecdotal report from 1979 to support the advice of avoidance.  Clinical trials using both chemotherapy and antioxidants seem to show increased patient survival. 

 

J Am Coll Nutr. 2005 Feb;24(1):16-21. Links

Chemotherapy alone vs. chemotherapy plus high dose multiple antioxidants in patients with advanced non small cell lung cancer.Pathak AK, Bhutani M, Guleria R, Bal S, Mohan A, Mohanti BK, Sharma A, Pathak R, Bhardwaj NK, Prasad KN, Kochupillai V.

Department of Medical Oncology, Institute Rotary Cancer Hospital, All India Institute of Medical Sciences, New Delhi 110 029, INDIA.

 

OBJECTIVE: In vitro and animal studies suggest that antitumor effect of chemotherapeutic agents may be enhanced by antioxidants. Therefore, we initiated a clinical study to test the efficacy of high-dose multiple antioxidants (vitamins C, E and beta carotene) as an adjunct to chemotherapy (paclitaxel and carboplatin) in non-small-cell lung cancer. METHODS: 136 patients of stage IIIb and stage IV NSCLC were randomized to receive chemotherapy (paclitaxel and carboplatin) alone (chemotherapy arm, n = 72) or chemotherapy in combination with ascorbic acid 6100 mg/day, dl-alpha-tocopherol (vitamin E) 1050 mg/day and beta-carotene 60 mg/day (combination arm, n = 64). Survival were calculated by the Kaplan-Meier method and compared using the log-rank test. RESULTS: An overall response rate (RR) of 33% was observed in chemotherapy arm with 24 patients showing a partial response (PR) and none showing a complete response (CR). In combination arm the overall RR was 37% with 24 patients showing PR and two showing CR. The median survival times in chemotherapy arm and combination arm were nine and 11 months respectively. The overall survival (OS) rates in chemotherapy arm and combination arm at one year were 32.9% and 39.1%, and at two years, 11.1% and 15.6% respectively. None of these differences were statistically significant (p = 0.20). Toxicity profiles were similar in both arms. CONCLUSIONS: These results do not support the concern that antioxidants might protect cancer cells from the free radical damage induced by chemotherapy. Larger trials are needed to demonstrate whether high-dose multiple antioxidants in conjunction with chemotherapy increase the response rates and/or survival time in advanced lung cancer.

 

PMID: 15670980 [PubMed - indexed for MEDLINE]

 

J Am Coll Nutr. 2003 Apr;22(2):118-23. Links

The use of antioxidants with first-line chemotherapy in two cases of ovarian cancer.Drisko JA, Chapman J, Hunter VJ.

Department of Obstetrics and Gynecology, Division of Gynecologic Oncology, University of Kansas Medical Center, 39012 Rainbow Boulevard, Kansas City, KS 66160, USA. jdrisko@kumc.edu

 

OBJECTIVE: Because of poor overall survival in advanced ovarian malignancies, patients often turn to alternative therapies despite controversy surrounding their use. Currently, the majority of cancer patients combine some form of complementary and alternative medicine with conventional therapies. Of these therapies, antioxidants, added to chemotherapy, are a frequent choice. METHODS: For this preliminary report, two patients with advanced epithelial ovarian cancer were studied. One patient had Stage IIIC papillary serous adenocarcinoma, and the other had Stage IIIC mixed papillary serous and seromucinous adenocarcinoma. Both patients were optimally cytoreduced prior to first-line carboplatinum/paclitaxel chemotherapy. Patient 2 had a delay in initiation of chemotherapy secondary to co-morbid conditions and had evidence for progression of disease prior to institution of therapy. Patient 1 began oral high-dose antioxidant therapy during her first month of therapy. This consisted of oral vitamin C, vitamin E, beta-carotene, coenzyme Q-10 and a multivitamin/mineral complex. In addition to the oral antioxidant therapy, patient 1 added parenteral ascorbic acid at a total dose of 60 grams given twice weekly at the end of her chemotherapy and prior to consolidation paclitaxel chemotherapy. Patient 2 added oral antioxidants just prior to beginning chemotherapy, including vitamin C, beta-carotene, vitamin E, coenzyme Q-10 and a multivitamin/mineral complex. Patient 2 received six cycles of paclitaxel/carboplatinum chemotherapy and refused consolidation chemotherapy despite radiographic evidence of persistent disease. Instead, she elected to add intravenous ascorbic acid at 60 grams twice weekly. Both patients gave written consent for the use of their records in this report. RESULTS: Patient 1 had normalization of her CA-125 after the first cycle of chemotherapy and has remained normal, almost 3(1/2) years after diagnosis. CT scans of the abdomen and pelvis remain without evidence of recurrence. Patient 2 had normalization of her CA-125 after the first cycle of chemotherapy. After her first round of chemotherapy, the patient was noted to have residual disease in the pelvis. She declined further chemotherapy and added intravenous ascorbic acid. There is no evidence for recurrent disease by physical examination, and her CA-125 has remained normal three years after diagnosis. CONCLUSION: Antioxidants, when added adjunctively, to first-line chemotherapy, may improve the efficacy of chemotherapy and may prove to be safe. A review of four common antioxidants follows. Because of the positive results found in these two patients, a randomized controlled trial is now underway at the University of Kansas Medical Center evaluating safety and efficacy of antioxidants when added to chemotherapy in newly diagnosed ovarian cancer.

 

PMID: 12672707 [PubMed - indexed for MEDLINE]

 

Gynecol Oncol. 2003 Mar;88(3):434-9. Links

The use of antioxidant therapies during chemotherapy.Drisko JA, Chapman J, Hunter VJ.

Department of Obstetrics and Gynecology, School of Medicine, University of Kansas Medical Center, Kansas City, KS 66160, USA. jdrisko@kumc.edu

 

OBJECTIVE: At the present time, many cancer patients combine some form of complementary and alternative medicine therapies with their conventional therapies. The most common choice of these therapies is the use of antioxidants. RESULTS: A review of four common antioxidants is undertaken, which includes vitamin E (mixed tocopherols and tocotrienols), beta-carotene (natural mixed carotenoids), vitamin C (ascorbic acid), and vitamin A (retinoic acid). Antioxidants act as electron acceptors as well as therapeutic biologic response modifiers. Despite the fact that chemotherapy-induced formation of free radicals is well-demonstrated, chemotherapy-induced cytotoxicity in general does not seem to depend on formation of reactive oxygen species. CONCLUSIONS: Currently, evidence is growing that antioxidants may provide some benefit when combined with certain types of chemotherapy. Because of the potential for positive benefits, a randomized controlled trial evaluating the safety and efficacy of adding antioxidants to chemotherapy in newly diagnosed ovarian cancer is underway at the University of Kansas Medical Center.

 

PMID: 12648599 [PubMed - indexed for MEDLINE]

 

Integr Cancer Ther. 2004 Dec;3(4):310-22. Links

Multiple dietary antioxidants enhance the efficacy of standard and experimental cancer therapies and decrease their toxicity.Prasad KN.

Center for Vitamin and Cancer Research, Department of Radiology, University of Colorado Health Sciences Center, Denver 80262-0278, USA. kedar.prasad@uchsc.edu

 

Cancer patients can be divided into 3 groups: those receiving standard or experimental therapy, those who have become unresponsive to these therapies, and those in remission at risk for recurrence or a second new cancer. While impressive progress in standard cancer therapy has been made, the value of this therapy in the management of solid tumors may have reached a plateau. At present, there is no strategy to reduce the risk of recurrence of the primary tumors or of a second cancer among survivors. Patients unresponsive to standard or experimental therapies have little option except for poor quality of life for the remainder of life. Therefore, additional approaches should be developed to improve the efficacy of current management of cancer. In this review, the author proposes that an active nutritional protocol that includes high doses of multiple dietary antioxidants and their derivatives (vitamin C, alpha-tocopheryl succinate, and natural beta-carotene), but not endogenously made antioxidants (glutathione- and antioxidant enzyme-elevating agents), when administered as an adjunct to radiation therapy, chemotherapy, or experimental therapy, may improve its efficacy by increasing tumor response and decreasing toxicity. This nutritional protocol can also be used when patients become unresponsive to standard therapy or experimental therapy to improve quality of life and possibly increase the survival time. The authors also propose that after completion of standard therapy and/or experimental therapy, a maintenance nutritional protocol that contains lower doses of antioxidants and their derivatives, together with modification in diet and lifestyle, may reduce the risk of recurrence of the original tumor and development of a second cancer among survivors. Experimental data and limited human studies suggest that use of these nutritional approaches may improve oncologic outcomes and decrease toxicity. This review also discusses the reasons for the current debates regarding the use of antioxidants during radiation or chemotherapy.

 

PMID: 15523102 [PubMed - indexed for MEDLINE]

 

Integr Cancer Ther. 2004 Dec;3(4):333-41. Links

Dietary antioxidants and human cancer.Borek C.

Department of Community Health and Family Medicine, Nutrition Infectious Disease Unit, Tufts University School of Medicine, Boston, Massachusetts 02111, USA. carmia.borek@tufts.edu

 

Epidemiological studies show that a high intake of anti-oxidant-rich foods is inversely related to cancer risk. While animal and cell cultures confirm the anticancer effects of antioxidants, intervention trials to determine their ability to reduce cancer risk have been inconclusive, although selenium and vitamin E reduced the risk of some forms of cancer, including prostate and colon cancer, and carotenoids have been shown to help reduce breast cancer risk. Cancer treatment by radiation and anticancer drugs reduces inherent antioxidants and induces oxidative stress, which increases with disease progression. Vitamins E and C have been shown to ameliorate adverse side effects associated with free radical damage to normal cells in cancer therapy, such as mucositis and fibrosis, and to reduce the recurrence of breast cancer. While clinical studies on the effect of anti-oxidants in modulating cancer treatment are limited in number and size, experimental studies show that antioxidant vitamins and some phytochemicals selectively induce apoptosis in cancer cells but not in normal cells and prevent angiogenesis and metastatic spread, suggesting a potential role for antioxidants as adjuvants in cancer therapy.

 

PMID: 15523104 [PubMed - indexed for MEDLINE]

 

Altern Ther Health Med. 2007 Mar-Apr;13(2):40-7.Links

Antioxidants and other nutrients do not interfere with chemotherapy or radiation therapy and can increase kill and increase survival, Part 2.Simone CB 2nd, Simone NL, Simone V, Simone CB.

Simone Protective Cancer Institute in Lawrenceville, NJ, USA.

 

PURPOSE: Some in the oncology community contend that patients undergoing chemotherapy and/or radiation therapy should not use food supplement antioxidants and other nutrients. Oncologists at an influential oncology institution contended that antioxidants interfere with radiation and some chemotherapies because those modalities kill by generating free radicals that are neutralized by antioxidants, and that folic acid interferes with methotrexate. This is despite the common use of amifostine and dexrazoxane, 2 prescription antioxidants, during chemotherapy and/or radiation therapy. DESIGN: To assess all evidence concerning antioxidant and other nutrients used concomitantly with chemotherapy and/or radiation therapy. The MEDLINE and CANCERLIT databases were searched from 1965 to November 2003 using the words vitamins, antioxidants, chemotherapy, and radiation therapy. Bibliographies of articles were searched. All studies reporting concomitant nutrient use with chemotherapy and/or radiation therapy (280 peer-reviewed articles including 62 in vitro and 218 in vivo) were indiscriminately included. RESULTS: Fifty human clinical randomized or observational trials have been conducted, involving 8,521 patients using beta-carotene; vitamins A, C, and E; selenium; cysteine; B vitamins; vitamin D3; vitamin K3; and glutathione as single agents or in combination. CONCLUSIONS: Since the 1970s, 280 peer-reviewed in vitro and in vivo studies, including 50 human studies involving 8,521 patients, 5,081 of whom were given nutrients, have consistently shown that do not interfere with therapeutic modalities for cancer. Furthermore, non-prescription antioxidants and other nutrients enhance the killing of therapeutic modalities for cancer, decrease their side effects, and protect normal tissue. In 15 human studies, 3,738 patients who took non-prescription antioxidants and other nutrients actually had increased survival.

 

PMID: 17405678 [PubMed - indexed for MEDLINE]

 

J Clin Oncol. 1999 Oct;17(10):3333-55. Links

Comment in:

J Clin Oncol. 2000 Aug;18(16):3064.

J Clin Oncol. 2000 May;18(9):2004-6.

J Clin Oncol. 2001 Jul 15;19(14):3439-41.

American Society of Clinical Oncology clinical practice guidelines for the use of chemotherapy and radiotherapy protectants.Hensley ML, Schuchter LM, Lindley C, Meropol NJ, Cohen GI, Broder G, Gradishar WJ, Green DM, Langdon RJ Jr, Mitchell RB, Negrin R, Szatrowski TP, Thigpen JT, Von Hoff D, Wasserman TH, Winer EP, Pfister DG.

American Society of Clinical Oncology, Health Services Research Department, Alexandria, VA 22314, USA. guideline@asco.org

 

PURPOSE: Because toxicities associated with chemotherapy and radiotherapy can adversely affect short- and long-term patient quality of life, can limit the dose and duration of treatment, and may be life-threatening, specific agents designed to ameliorate or eliminate certain chemotherapy and radiotherapy toxicities have been developed. Variability in interpretation of the available data pertaining to the efficacy of the three United States Food and Drug Administration-approved agents that have potential chemotherapy- and radiotherapy-protectant activity-dexrazoxane, mesna, and amifostine-and questions about the role of these protectant agents in cancer care led to concern about the appropriate use of these agents. The American Society of Clinical Oncology sought to establish evidence-based, clinical practice guidelines for the use of dexrazoxane, mesna, and amifostine in patients who are not enrolled on clinical treatment trials. METHODS: A multidisciplinary Expert Panel reviewed the clinical data regarding the activity of dexrazoxane, mesna, and amifostine. A computerized literature search was performed using MEDLINE. In addition to reports collected by individual Panel members, all articles published in the English-speaking literature from June 1997 through December 1998 were collected for review by the Panel chairpersons, and appropriate articles were distributed to the entire Panel for review. Guidelines for use, levels of evidence, and grades of recommendation were reviewed and approved by the Panel. Outcomes considered in evaluating the benefit of a chemotherapy- or radiotherapy-protectant agent included amelioration of short- and long-term chemotherapy- or radiotherapy-related toxicities, risk of tumor protection by the agent, toxicity of the protectant agent itself, quality of life, and economic impact. To the extent that these data were available, the Panel placed the greatest value on lesser toxicity that did not carry a concomitant risk of tumor protection. RESULTS AND CONCLUSION: Mesna: (1) Mesna, dosed as detailed in these guidelines, is recommended to decrease the incidence of standard-dose ifosfamide-associated urothelial toxicity. (2) There is insufficient evidence on which to base a guideline for the use of mesna to prevent urothelial toxicity with ifosfamide doses that exceed 2.5 g/m(2)/d. (3) Either mesna or forced saline diuresis is recommended to decrease the incidence of urothelial toxicity associated with high-dose cyclophosphamide use in the stem-cell transplantation setting. Dexrazoxane: (1) The use of dexrazoxane is not routinely recommended for patients with metastatic breast cancer who receive initial doxorubicin-based chemotherapy. (2) The use of dexrazoxane may be considered for patients with metastatic breast cancer who have received a cumulative dosage of 300 mg/m(2) or greater of doxorubicin in the metastatic setting and who may benefit from continued doxorubicin-containing therapy. (3) The use of dexrazoxane in the adjuvant setting is not recommended outside of a clinical trial. (4) The use of dexrazoxane can be considered in adult patients who have received more than 300 mg/m(2) of doxorubicin-based therapy for tumors other than breast cancer, although caution should be used in settings in which doxorubicin-based therapy has been shown to improve survival because of concerns of tumor protection by dexrazoxane. (5) There is insufficient evidence to make a guideline for the use of dexrazoxane in the treatment of pediatric malignancies, with epirubicin-based regimens, or with high-dose anthracycline-containing regimens. Similarly, there is insufficient evidence on which to base a guideline for the use of dexrazoxane in patients with cardiac risk factors or underlying cardiac disease. (6) Patients receiving dexrazoxane should continue to be monitored for cardiac toxicity. Amifostine: (1) Amifostine may be considered for the reduction of nephrotoxicity in patients receiving cisplatin-based chemoth

 

PMID: 10506637 [PubMed - indexed for MEDLINE]

 

J Int Med Res. 2005 Nov-Dec;33(6):687-92. Links

Oxidant/antioxidant parameters and their relationship with chemotherapy in Hodgkin's lymphoma.Kaya E, Keskin L, Aydogdu I, Kuku I, Bayraktar N, Erkut MA.

Department of Haematology, Faculty of Medicine, Inonu University, Malatya, Turkey. ekaya@inonu.edu.tr

 

This study investigated changing levels of serum oxidant/antioxidant with chemotherapy and their relation to treatment in 34 Hodgkin's lymphoma patients. The patient population consisted of 19 males and 15 females. Mean age was 30.41 +/- 12.08 years. All patients received the adriamycin, bleomycin, vincristine and dexamethasone (ABVD) treatment protocol. Blood samples were taken before treatment, and on days 1 and 7 during treatment for measurement of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), malondialdehyde (MDA), nitric oxide (NO) and enzyme activities. After ABVD treatment, mean free radical levels were increased and antioxidant levels were significantly decreased in the serum. ABVD treatment results in an increase of free radical levels and a decrease of antioxidant levels in the serum of patients with Hodgkin's lymphoma.

 

PMID: 16372587 [PubMed - indexed for MEDLINE]

 

Eksp Onkol. 1986;8(2):63-5.Links

[Effect of ascorbic acid on the development of a spontaneous lymphoproliferative process in SJL/J-strain mice][Article in Russian]

 

 

Korytova LI, Gubareva AV.

Ascorbic acid (AA) effects on the development of lymphoproliferative process according to the type of a reticular variant of Hodgkin's disease have been investigated in SJL/J mice. An oral AA injection in a 0.05% aqueous solution for 6-8 months (0.625 mg/kg) with a total dose of 0.5 per mouse has not produced any side effects, has reduced both the rate of tumour process development (from 80.5% in control to 68.0% in experiment) and the degree of its extension, and also has led to a statistically significant decrease in the frequency of development of general amyloidosis.

 

PMID: 3698884 [PubMed - indexed for MEDLINE]

 

Scott Med J. 1979 Apr;24(2):151-3.Links

Acute reactions to mega ascorbic acid therapy in malignant disease.Campbell A, Jack T.

Three cases are described, 2 of Hodgkin's disease and a further case of bronchial carcinoma, where high dosage ascorbic acid treatment appeared to be associated with the development of potentially dangerous symptoms. It is suggested that mega ascorbic acid therapy should be given with caution in malignant disease, with a slow build-up over several days to high levels of dosage.

 

PMID: 227054 [PubMed - indexed for MEDLINE]

 

J Pediatr Hematol Oncol. 2007 Aug;29(8):519-22. Links

Hair selenium status in children with leukemia and lymphoma.Ozgen IT, Dagdemir A, Elli M, Saraymen R, Pinarli FG, Fisgin T, Albayrak D, Acar S.

Divisionsof Pediatric Oncology, Ondokuz Mayis University, Medical Faculty, Samsun, Turkey. drtolgaozgen@yahoo.com

 

Selenium (Se) is a trace element contributing to the structure of antioxidant system that saves cells from reactive oxygen species. Low serum Se levels have been reported in pediatric and adult patients with cancers. On the other hand, hair Se levels, predicting the long-term body Se status, have been reported in only adult patients with cancer. The aim of the study was to investigate the hair Se status in children with newly diagnosed lymphoid malignancies and the relation between malnutrition and Se deficiency. Thirty patients with leukemia (n=17) and lymphoma (n=13), and 25 healthy controls were enrolled to the study. Se was determined with atomic absorption spectrophotometrical method. Hair Se levels of the patients were significantly lower than those of control group [666.96+/-341.46 ng/g vs. 1019.22+/-371.83 ng/g (P<0.001)]. Children with lymphoma had lower Se than the children with acute lymphoblastic leukemia but not statistically significant [547.03+/-283.67 ng/g vs. 758.67+/-361.05 ng/g (P>0.05)]. Malnourished patients (11/30) had lower hair Se levels (483.51+/-235.55 ng/g) than those of the controls (P=0.036), whereas the Se levels of the patients who had no malnutrition (773.17+/-352.92 ng/g) were also lower than those of the controls but not statistically significant (P=0.053). There was no correlation between age, sex, and the hair Se levels. In this study, we found that hair Se levels of the children with leukemia and lymphoma, especially those of malnourished patients, were lower than those of controls. Additional studies are needed to determinate whether low levels of hair Se may play a role in carcinogenesis.

 

PMID: 17762491 [PubMed - indexed for MEDLINE]

 

Leuk Lymphoma. 2000 Nov;39(5-6):555-62.Links

High prevelance of chronic magnesium deficiency in T cell lymphoblastic leukemia and chronic zinc deficiency in children with acute lymphoblastic leukemia and malignant lymphoma.Sahin G, Ertem U, Duru F, Birgen D, Yüksek N.

Dr. Sami Ulus Children's Hospital Department of Pediatric Oncology, Ankara, Turkey.

 

Magnesium and zinc are the elements having essential roles in regulation of cell growth, division and differentiation. There have been some studies in the literature suggesting an association between the deficiency of these elements and the development of malignant disorders. In this study hair and serum zinc and magnesium levels were investigated in children with acute lymphoblastic leukemia (ALL) and malignant lymphoma (ML) at the time of initial diagnosis. Ten children with T-cell ALL, 10 children with B-precursor ALL, 5 children with Burkitt's Lymphoma (BL), 11 children with Hodgkin's lymphoma (HL), 10 children with non-Burkitt non-Hodgkin's lymphoma (NBNHL) and 12 age and sex matched healthy children as a control group were included in the study. Mean hair magnesium levels in all of the groups of the patients were lower than the levels in the control group but the difference was statistically significant only in the children with T cell ALL comparable to the controls (28.9+/-3.9 microg/g and 87.6+/-18.5 microg/g respectiveley, p<0,05). Mean serum magnesium levels in all the cohorts were not significantly different than those in controls (p>0.05 in each comparison). Mean hair zinc levels in the patients with T-cell, B-precursor ALL, BL, HL, NBNHL were 103.4+/-14.6 microg/g, 100.9+/-7.8 microg/g, 91.1+/-19 microg/g, 72.5+/-9.1 microg/g, 103.2+/-12.2 microg/g respectively. Each of these levels were significantly lower than the mean hair zinc levels of the control group (141.2+/-9.6 microg/g, p<0.05 in each comparison). Although mean serum zinc levels in all of the groups were also decreased, the differences were statistically significant only in the groups with B-precursor ALL, HL and NBNHL (75.9+/-5.29 microg/dl, 68.6+/-7.3 microg/dl, 85.7+/-5.5 microg/dl respectively) when compared with controls (105.1+/-9.9 microg/dl, p<0.05 in each comparison). Hair magnesium and zinc levels showed a positive correlation with each other in all the groups (r congruent with 0.5). No significant difference was found in the mean hair/serum magnesium and zinc levels between malnourished and nonmalnourished patients. In conclusion, regarding the results of our study and previous data in the literature chronic magnesium and zinc deficiency seems to be associated with the development of ALL and malignant lymphoma in a group of patients.

 

PMID: 11342338 [PubMed - indexed for MEDLINE]

 

Clin Biochem. 2000 Apr;33(3):209-12. Links

Lipid peroxidation and antioxidant system in the blood of patients with Hodgkin's disease.Güven M, Oztürk B, Sayal A, Ozet A.

Department of Medical Biology, Cerrahpasa Medical Faculty, Istanbul University, Istanbul, Turkey. mgguven@istanbul.edu.tr

 

OBJECTIVES: The purpose of this study was to measure the extent of lipid peroxidation and the status of antioxidants in patients with Hodgkin's disease.DESIGN AND METHODS: Glutathione peroxidase (GPX) and superoxide dismutase (SOD) activities, and malondialdehyde (MDA), selenium, zinc and copper content have been measured in 20 patients with Hodgkin's disease and 30 age-matched controls.RESULTS: Significantly higher concentrations of MDA in plasma as well as in erythrocytes were found compared to the control group. In both plasma and erythrocytes, GPX activity, selenium and zinc levels were significantly lower in patients than in controls. However, SOD activity in erythrocytes and copper levels in both plasma and erythrocytes were significantly higher in patients.CONCLUSION: We conclude that the antioxidant system is impaired in Hodgkin's disease due to the abnormal metabolism of trace elements and antioxidant enzymes.

 

PMID: 10913520 [PubMed - indexed for MEDLINE]

 

Br J Haematol. 1987 Mar;65(3):347-50.Links

Superoxide dismutase, glutathione peroxidase and catalase in the red cells of patients with malignant lymphoma.Bewick M, Coutie W, Tudhope GR.

Erythrocyte superoxide dismutase, glutathione peroxidase and catalase activities have been measured in patients with untreated malignant lymphomas. Marked deficiencies of superoxide dismutase (P less than 0.001) and glutathione peroxidase (P less than 0.001) were found, whereas catalase levels were normal. There was no apparent difference in enzyme activities between the different histological types of lymphoma.

 

PMID: 3567087 [PubMed - indexed for MEDLINE]

 

Clin Exp Immunol. 1981 Nov;46(2):313-20. Links

Evidence for the involvement of monocyte-derived toxic oxygen metabolites in the lymphocyte dysfunction of Hodgkin's disease.Deshazo RD, Ewel C, Londono S, Metzger Z, Hoffeld JT, Oppenheim JJ.

This study was performed to see if adherent cell-derived toxic oxygen metabolites contribute to the suppression of mononuclear cell blastogenic responses in Hodgkin's disease. Peripheral blood mononuclear cells from 10 patients with Hodgkin's disease were stimulated in culture with the mitogen PHA in the presence of the prostaglandin inhibitor indomethacin and the antioxidants catalase or vitamin E. Patient lymphocytes showed significant increases in PHA-induced proliferation at all PHA doses when cultured with indomethacin. Further augmentation of lymphocyte proliferation was achieved with the addition of catalase or vitamin E to indomethacin in the culture system. The increases in proliferation seen on culture with these agents were greatest in patients with more depressed initial PHA responses. When adherent cells were removed before culture, the agents no longer facilitated increases in proliferation. These data suggest that abnormal lymphocyte proliferative responses seen in Hodgkin's disease may result in part from the excessive production of toxic oxygen metabolites as well as prostaglandins by adherent cell populations.

 

PMID: 7337972 [PubMed - indexed for MEDLINE]

 

 

 

 

 
 

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