Carotenoids induce morphological changes in human mammary epithelial cell cultures

Rock, Cheryl L.; Kusluski, Robin A.; Galvez, Marina; Ethier, Stephen P.

doi:10.1080/01635589509514386

Cited by 44 publications

(16 citation statements)

References 26 publications

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“…An accumulation of 0.004 nmol/lO%ells was found when 7 pM $-carotene was added to MCFlOA human mammary epithelial cells for five days (43). These cellular concentrations are within the range reported in similar studies using different cell lines.…”

Section: Discussionsupporting

confidence: 84%

Subcellular Accumulation of β-Carotene and Retinoids in Growth-Inhibited NCI-H69 Small Cell Lung Cancer Cells

Prakash¹,

Jackson²,

Gerber³

1999

Nutrition and Cancer

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Delivery of beta-carotene in tetrahydrofuran slowed the growth of NCI-H69 small cell lung cancer cells. Analysis of cells and cellular fractions revealed that beta-carotene-treated cells accumulated beta-carotene as well as some polar metabolites, primarily in the crude nuclei. Cells were grown at 1 x 10(5) cells/ml and treated with 20 microM beta-carotene. Growth monitoring up to 15 days indicated an inverse relationship between the duration of beta-carotene treatment and the rate of cell growth. Reverse-phase high-performance liquid chromatography analysis of treated cells showed the presence of beta-carotene, retinoic acid, retinol, and retinal, with beta-carotene accounting for the major material recovered. When cellular fractions were analyzed for beta-carotene, it was found to be located primarily in the crude nuclei. These results demonstrate that treatment of small cell lung cancer cells with beta-carotene results in a reduced growth of the cells. Further investigation is required to show a direct effect of beta-carotene or its intracellular polar metabolites on these cells. Accumulation of beta-carotene in the nucleus suggests a need for evaluating the nuclear role for beta-carotene.

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Section: Discussionsupporting

confidence: 84%

Subcellular Accumulation of β-Carotene and Retinoids in Growth-Inhibited NCI-H69 Small Cell Lung Cancer Cells

Prakash¹,

Jackson²,

Gerber³

1999

Nutrition and Cancer

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“…While there is good evidence from cell-culture and animal studies supporting the role of dietary components in mammary cell tumorigenesis [14][15][16] results from studies in women have been variable. Red meat intake has been hypothesized to increase breast cancer risk, but while case-control and ecologic studies have supported a positive association, prospective cohort studies have been inconsistent.…”

Section: Introductionmentioning

confidence: 91%

Is red meat intake a risk factor for breast cancer among premenopausal women?

Taylor¹,

Misra

Mukherjee³

2009

Breast Cancer Res Treat

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Breast cancer is the second leading cause of cancer deaths in women today and is the most common cancer among women. Although a number of risk factors such as genetics, family history, parity, age at first birth, and age at menarche and menopause have been established, most are difficult to modify. Diet, however, is a potentially modifiable approach for prevention and a variety of dietary patterns have been examined with respect to their role in breast cancer. One such dietary factor is red meat consumption. Red meat intake has been hypothesized to increase breast cancer risk but while both case-control and ecologic studies have supported a positive association, prospective cohort studies have been inconsistent. One explanation for this inconsistency may be related to menopausal status. We performed a meta-analysis on the association between breast cancer risk and red meat consumption in premenopausal women. A total of ten studies were identified. The summary relative risk was 1.24 (95% CI 1.08-1.42). Case-control studies (N = 7) had a risk of 1.57 (95% CI 1.23-1.99), while cohort studies (N = 3) had a summary relative risk of 1.11 (95% CI 0.94-1.31).

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“…Zhi et al (2000) showed that newborn rat calvarial osteoblastic cells cultured in all-trans retinoic acid for 24 h up-regulate the proliferation of osteoblasts. Rock et al (1995) noted that carotenoids promote human mammary epithelial cell proliferation and differentiation. In the current study, cell proliferation was significantly improved when BMEC were treated with VA, which is consistent with previous results.…”

Section: Discussionmentioning

confidence: 99%

Vitamin A affects the expression of antioxidant genes in bovine mammary epithelial cells with oxidative stress induced by diethylene triamine-nitric oxide

Shi¹,

Yan²,

Jin³

et al. 2016

CZECH J ANIM SCI

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ABSTRACT:The considerable increase in oxygen requirements due to the high metabolic rate of the bovine mammary epithelial cells (BMEC) during lactation results in an augmented production of reactive nitrogen species (RNS), such as nitric oxide (NO), which may expose cows to increased oxidative stress. Vitamin A (VA) has been shown in several studies to enhance the antioxidant defence system against oxidative stress, but whether the reason is related to a reduced NO production remains unclear. Diethylene triamine-nitric oxide polymer (NOp) is a type of NO-generating compound, which is safe, efficacious, and releases NO over a long period. The current study was conducted to investigate the effect of VA on the antioxidant function in BMEC and the underlying mechanism by discussing the protection of VA on NO-induced oxidative stress of BMEC. The experiment was conducted using a single-factor completely randomized arrangement. Primary BMEC were isolated from the mammary glands of Holstein dairy cows. The third generation cells were randomly divided into four equal groups with six replicates each. Each group received different combinations of VA and NOp treatment as follows: controls (without VA and NOp), NOp treatment alone, VA treatment alone, and VA and NOp treatment together. The lysates were collected to evaluate the activities of glutathione peroxidase (GPx) and thioredoxin reductase (TrxR) and the contents of reactive oxygen species (ROS) and malondialdehyde (MDA), and the cell-free supernatants were collected to analyze selenoprotein P (SelP) content, inducible nitric oxide synthase (iNOS) activities and nitric oxide (NO), interleukin-1 (IL-1), interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α) contents. The results suggested that compared to the control, the cell proliferation, the activity of the antioxidants GPx and TrxR, the content of SelP and the antioxidant gene expressions of GPx1, GPx4, and TrxR1 were significantly decreased (P < 0.05), and the contents of ROS and MDA, the activity of iNOS, the contents of NO and IL-1, IL-6, TNF-α, and their mRNA expressions were increased dramatically in the NOp treatment alone group (P < 0.05), but the opposite changes were observed in the VA treatment alone group. Compared to the NOp treatment alone, the VA and NOp treatment together significantly improved cell proliferation, the activities of the antioxidants GPx and TrxR, and the gene expressions of GPx1 and TrxR1, and dramatically decreased the contents of ROS and MDA, the activity of iNOS, the contents of NO and IL-1, IL-6, TNF-α and their mRNA expression levels (P < 0.05). The present research suggests that VA can improve the antioxidant function of BMEC and protect the cells from experiencing the NOp-induced oxidative stress by regulating antioxidant gene expression. The probable mechanism is that VA can reduce the activity of iNOS and its mRNA expression by down-regulating of the expression of IL-1, IL-6, and TNF-α to reduce NO production. However, the exact mechanism warrants future exploration. Keyword...

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Carotenoids induce morphological changes in human mammary epithelial cell cultures

Cited by 44 publications

References 26 publications

Subcellular Accumulation of β-Carotene and Retinoids in Growth-Inhibited NCI-H69 Small Cell Lung Cancer Cells

Subcellular Accumulation of β-Carotene and Retinoids in Growth-Inhibited NCI-H69 Small Cell Lung Cancer Cells

Is red meat intake a risk factor for breast cancer among premenopausal women?

Vitamin A affects the expression of antioxidant genes in bovine mammary epithelial cells with oxidative stress induced by diethylene triamine-nitric oxide

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