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Beta carotene is associated with the regression of hamster buccal pouch carcinoma and the induction of tumor necrosis factor in macrophages.
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Beta carotene (250 micrograms/ml) dissolved in mineral oil applied either topically or injected locally (190 ng/ml dissolved in media) into DMBA (7,12-dimethylbenz(a)anthracene)-induced or HCPC-1 cell line-produced oral squamous cell carcinoma of the hamster buccal pouch was observed to result in
β-Carotene accumulation in 3T3-L1 adipocytes inhibits the elevation of reactive oxygen species and the suppression of genes related to insulin sensitivity induced by tumor necrosis factor-α.
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OBJECTIVE
β-Carotene is an abundant carotenoid with potent antioxidative activities and accumulates in adipose tissue. However, its physiologic functions are poorly understood. In this study, we examined whether accumulation of β-carotene for 4 d in insulin-resistant 3T3-L1 adipocytes alters the
Tumor necrosis factor in experimental cancer regression with alphatocopherol, beta-carotene, canthaxanthin and algae extract.
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Regression of established hamster buccal pouch carcinoma has recently been demonstrated in association with an induction of tumor necrosis factor alpha in macrophages. Regression of hamster buccal pouch tumors has also been demonstrated following the local injection of alphatocopherol, canthaxanthin
Dietary beta-carotene supplementation modulates the production of tumour necrosis factor-alpha by human monocytes.
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β-Carotene down-regulates inducible nitric oxide synthase gene expression and induces apoptosis by suppressing bcl-2 expression and activating caspase-3 and p53 genes in B16F-10 melanoma cells
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The objective of this research was to assess the effect of β-carotene on the regulation of nitric oxide (NO) and tumor necrosis factor (TNF)-α production and stimulation of apoptosis in B16F-10 melanoma cells. β-Carotene at a concentration of 10 μg/mL could significantly (P < .01) inhibit NO and
Antioxidant effect of beta-carotene in cystic fibrosis and bronchiectasis: clinical and laboratory parameters of a pilot study.
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The carotenoids are potent antioxidants with the ability to quench singlet oxygen and other toxic oxygen species. The aim of this pilot study was to investigate the protective effect of beta-carotene on oxidant system in patients with cystic fibrosis (CF) and in patients with bronchiectasis (BE)
Cytotoxicity of β-carotene cleavage products and its prevention by antioxidants.
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When we investigated the genotoxicity of beta-carotene cleavage products (CPs) in primary rat hepatocytes stimulated to proliferate, we observed dose-dependent increases of chromosomal aberrations, sister chromatid exchanges and micronuclei. In contrast to other genotoxic substances, however, this
Interactions of beta-carotene and flavonoids on the secretion of pro-inflammatory mediators in an in vitro system.
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Chronic inflammation, a process linked to increased oxidative stress, may induce many diseases. Whether beta-carotene prevents inflammation is unclear. Using phorbol-12-myristate-13-acetate (PMA)-stimulated HL-60 cells, we investigated the effects of 2 or 20 microM beta-carotene on the inflammatory
Beta-carotene prevents ozone-induced proinflammatory markers in murine skin.
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Beta-carotene has been thought to protect against oxidative stress generated by ultraviolet radiation and thus prevents skin cancer and skin aging (Biesalski and Obermueller-Jevic, 2001). However, nothing is known about its potential effects against other environmental sources of oxidative stress
Liver necrosis induced by acute intraperitoneal ethanol administration in aged rats.
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It is generally agreed that the deleterious pathophysiological effects of ethanol are caused, at least partially by an increase in free radical production. However, little attention has been directed to the effects of ethanol upon elderly organisms. Male Wistar rats at ages 3, 6, 12, 18 and 24
Omega-3 fatty acids enhance tumor necrosis factor-alpha levels in heart transplant recipients.
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BACKGROUND
Proinflammatory cytokines may contribute to clinical complications in heart transplant (HTx) recipients. Previous studies have shown immunomodulating effects of omega-3 fatty acids, but the results are somewhat conflicting. In this study, we examined plasma levels of tumor necrosis factor
Effects of retinoic acid (vitamin A) on tumor necrosis factor cytolytic action.
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Tumor necrosis factor (TNF) is a monokine produced primarily by macrophages. TNF has a number of activities including direct lysis of certain transformed cells and induction of antiviral activity. One of the protoypical transformed cell lines used for studying TNF cytolysis is murine L-929 cells.
The antiapoptotic effects of different doses of β-carotene in chronic ethanol-fed rats.
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BACKGROUND
Ethanol consumption might induce hepatic apoptosis and cause liver damage. The study was to investigate the effects of different doses of β-carotene supplementation on the antioxidant capacity and hepatic apoptosis in chronic ethanol-fed rats.
METHODS
Rats were divided into 6 groups: C
Eat more carrots? Dampening cell death in ethanol-induced liver fibrosis by β-carotene.
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Alcoholic liver disease (ALD) represents one of the principal causes of liver damage in humans. Long-term ethanol abuse leads to progressive liver injury and tissue remodeling, including steatosis, inflammation, fibrosis, cirrhosis and increased risk for hepatocellular carcinoma (HCC) development.
The effect of beta-carotene supplementation on the immune function of blood monocytes from healthy male nonsmokers.
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Although there is strong epidemiologic evidence that diets rich in carotenoids such as beta-carotene are associated with a reduced incidence of cancer, the cellular mechanisms underlying this phenomenon remain unknown. This article describes the effect of dietary beta-carotene supplementation on
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