Italian multicenter study on the safety and efficacy of coenzyme Q10 as adjunctive therapy in heart failure

Baggio, E.; Gandini, R; Plancher, Angelo Cesare; Passeri, M; Carmosino, G

doi:10.1016/0098-2997(94)90040-x

Cited by 116 publications

(76 citation statements)

References 6 publications

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“…These potential effects on cancer could reside in the double role of CoQ 10 at the mitochondrial level as redox carrier and potent antioxidant molecule. Other supporting evidence for the CoQ 10 effect includes protection of cells from the toxicity of chemotherapy (24,25) and stimulation of the immune system against diseases (26,27). In addition, CoQ 10 has been seen to inhibit proliferation of cancer cells in vitro (28) and the growth of cancer cells transplanted into rats and mice (29,30).…”

Section: Discussionmentioning

confidence: 99%

Identification and Characterization of a Novel Melanoma Tumor Suppressor Gene on Human Chromosome 6q21

Fung¹,

Smith²,

Brown³

et al. 2009

Clinical Cancer Research

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Purpose: By characterizing a complex chromosome rearrangement involving 6q and 17p in melanoma cell line UACC-930, we isolated a candidate tumor suppressor gene at 6q21, named prenyl diphosphate synthase subunit 2 (PDSS2), which was interrupted by an inversion breakpoint. The purpose of this study was to determine the tumor-suppressive potential of PDSS2 in the development of melanoma. Experimental Design: To isolate the rearranged 6q in UACC-930 cells, a bacterial artificial chromosome clone (RP1-67A8) covering the breakpoint at 6q21 was digested with HindIII and each DNA fragment was used as the probe for the breakpoint in Southern blotting. The HindIII fragment probe covering the breakpoint was then used to screen an EcoRI-digested DNA library generated from UACC-930. To characterize the tumor-suppressive potential of PDSS2, PDSS2 was stably transfected into a highly tumorigenic melanoma cell line, UACC-903. The tumor-suppressive function of PDSS2 was shown by both in vitro and in vivo assays. The differential expression of PDSS2 in benign nevi and primary melanoma samples was also studied. Results: Down-regulation of PDSS2 was observed in 59 of 87 (67.8%) primary melanomas, which was significantly higher than that in benign nevi (7 of 66, 10.6%; P < 0.001). In addition, an overexpression of the PDSS2 in UACC-903 cells could inhibit tumor cell growth, decrease the colony-forming ability in soft agar, and totally abrogate the tumorigenicity of UACC-903 in nude mice. Conclusions: Our results support the proposal that PDSS2 is a novel tumor suppressor gene that plays an important role in the development of malignant melanoma.Melanoma is the most serious type of skin cancer (1). Genetic alterations in melanoma have been widely studied and the deletion of 6q is one of the most common chromosomal changes (2 -4). The reversion of the tumorigenic phenotype of melanoma cells by introducing a normal human chromosome 6 provides the first biological evidence that chromosome 6 contains a tumor suppressor gene (TSG) associated with melanoma pathogenesis (5). The abnormality of 6q has also been detected in other malignancies, including malignant lymphoma (6), ovarian (7), and prostate carcinomas (8).Several studies showed that 6q21 is the most frequent deleted region, suggesting the existence of a TSG at 6q21 (2, 3, 9). Although a couple of candidate TSGs at 6q, including AIM1 at 6q21 (10) and SOD2 at 6q25.3 (11), has been studied, the underlying mechanisms of these genes in melanoma development are unclear. In addition, the tumor-suppressive role of SOD2 is controversial. Miele et al. (12) found that SOD2 could not suppress tumorigenicity or metastasis of human melanoma C8161 cells. Therefore, more effort in looking for new candidate TSGs at 6q related to melanoma pathogenesis is justified.In our previous study, we found a reciprocal-like translocation between 6q21 and 17p13 in the melanoma cell line UACC-930 (9). The translocation was further characterized by chromosome microdissection and fluorescence in situ h...

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Section: Discussionmentioning

confidence: 99%

Identification and Characterization of a Novel Melanoma Tumor Suppressor Gene on Human Chromosome 6q21

Fung¹,

Smith²,

Brown³

et al. 2009

Clinical Cancer Research

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“…Many studies have confirmed that CoQ 10 is safe. One of them, which evaluated the effects of CoQ 10 supplementation on 2500 patients diagnosed with congestive heart failure (50-150 mg of CoQ 10 daily for three months), reported that the patients showed a remarkable improvement in clinical signs and symptoms, without adverse side effects (Baggio et al 1994). This study and many others conclude that CoQ 10 supplementation is safe and effective.…”

Section: Coq 10 and Diseasesmentioning

confidence: 99%

Nourishing and health benefits of coenzyme Q<sub>10</sub>

Borekova¹,

Hojerová²,

Koprda³

et al. 2008

Czech J. Food Sci.

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“…In a study of 3500 patients given CoQ 10 for up to seven years, adverse effects were minor and occurred in only 0.8%. 26 Study limitations Differences in exclusion criteria, age, therapy duration and use of concomitant therapy. In the studies included in the meta-analysis, there were differences between patient populations with respect to age, underlying disease and comorbidities.…”

Section: Side Effectsmentioning

confidence: 99%

Coenzyme Q10 in the treatment of hypertension: a meta-analysis of the clinical trials

et al. 2007

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Our objective was to review all published trials of coenzyme Q 10 for hypertension, assess overall efficacy and consistency of therapeutic action and side effect incidence. Meta-analysis was performed in 12 clinical trials (362 patients) comprising three randomized controlled trials, one crossover study and eight open label studies. In the randomized controlled trials (n ¼ 120), systolic blood pressure in the treatment group was 167.7 (95% confidence interval, CI: 163.7-171.1) mm Hg before, and 151.1 (147.1-155.1) mm Hg after treatment, a decrease of 16.6 (12.6-20.6, Po0.001) mm Hg, with no significant change in the placebo group. Diastolic blood pressure in the treatment group was 103 (101-105) mm Hg before, and 94.8 (92.8-96.8) mm Hg after treatment, a decrease of 8.2 (6.2-10.2, Po0.001) mm Hg, with no significant change in the placebo group. In the crossover study (n ¼ 18), systolic blood pressure decreased by 11 mm Hg and diastolic blood pressure by 8 mm Hg (Po0.001) with no significant change with placebo. In the open label studies (n ¼ 214), mean systolic blood pressure was 162 (158.4-165.7) mm Hg before, and 148.6 (145-152.2) mm Hg after treatment, a decrease of 13.5 (9.8-17.1, Po0.001) mm Hg. Mean diastolic blood pressure was 97.1 (95.2-99.1) mm Hg before, and 86.8 (84.9-88.8) mm Hg after treatment, a decrease of 10.3 (8.4-12.3, Po0.001) mm Hg. We conclude that coenzyme Q 10 has the potential in hypertensive patients to lower systolic blood pressure by up to 17 mm Hg and diastolic blood pressure by up to 10 mm Hg without significant side effects.

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Italian multicenter study on the safety and efficacy of coenzyme Q10 as adjunctive therapy in heart failure

Cited by 116 publications

References 6 publications

Identification and Characterization of a Novel Melanoma Tumor Suppressor Gene on Human Chromosome 6q21

Identification and Characterization of a Novel Melanoma Tumor Suppressor Gene on Human Chromosome 6q21

Nourishing and health benefits of coenzyme Q<sub>10</sub>

Coenzyme Q10 in the treatment of hypertension: a meta-analysis of the clinical trials

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