Carotenoid derivatives inhibit nuclear factor kappa B activity in bone and cancer cells by targeting key thiol groups

Linnewiel-Hermoni, Karin; Motro, Yair; Miller, Yifat; Levy, Joseph; Sharoni, Yoav

doi:10.1016/j.freeradbiomed.2014.07.024

Cited by 71 publications

(61 citation statements)

References 77 publications

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“…Although, in a U.S. case-control study consuming beta-carotene and total carotenoids was associated with a reduced risk of lung cancer (20). Generally, in many studies, it is reported that the serum levels of carotenoids were negatively associated with lung cancer risk (17,20,42). …”

Section: Discussionmentioning

confidence: 96%

“…Via their antioxidant action, 2 major antioxidants, lycopene and beta-carotene, may reduce the risk of lung cancer in human (17). It has been reported that the use of carotenoids are higher, and their efficiency is reduced in cancer (36), or other inflammatory situations (37).…”

Section: Discussionmentioning

confidence: 99%

“…The protective effect of antioxidant-rich carotenoids may explain this inverse association (16). Several recent studies have found some new anticarcinogenic mechanisms by which carotenoids induce the inhibition of the activity of nuclear factor kappa B (NFkB), and also exert antiprolifrative and apoptotic activities (17)(18)(19). Human body cannot synthesize carotenoids; therefore, it depends on the dietary or supplementary intake (20).…”

Section: Introductionmentioning

confidence: 99%

“…Lycopene has the most potential antioxidant effect among carotenoids (23,24), and beta-carotene is the most abundant carotenoid in the human body (25). Therefore, it is expected these 2 carotenoids play a key beneficial role in reducing the risk of lung cancer (17). The vast majority of current evidence on associations of dietary pattern with lung cancer is derived from populations in North America and Europe.…”

Section: Introductionmentioning

confidence: 99%

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Dietary Intake and Serum Level of Carotenoids in Lung Cancer Patients: A Case-Control Study

Asbaghi

Saedisomeolia

Hosseini

et al. 2015

Nutrition and Cancer

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The aim of this study was to compare the dietary intake and serum levels of some selected carotenoids of lung cancer patients with healthy subjects. Thirty-five lung cancer patients and 33 healthy people were enrolled into this case-control study. Daily intake of nutrients was estimated using a semiquantitative food frequency questionnaire and a 3-day 24-h food recall questionnaire. The concentration of serum beta-carotene and lycopene were analyzed using a high performance liquid chromatography method. Case and control groups did not differ by the means of age, gender, smoking habits, weight, body mass index, mean daily energy intake, mean daily fat intake, and the percentage of daily energy provided by fat to total daily energy intake. The beta-carotene and lycopene intake of the case subjects was 96% and 195% greater than that of the control subjects. Daily intake of fruits and vegetables in the cancer group was higher than the control group. However, the serum concentration of 118% beta-carotene and 60% lycopene were higher in the control group. Despite a higher daily dietary intake of beta-carotene and lycopene by lung cancer patients, serum beta-carotene and lycopene concentrations were significantly lower than the group without cancer.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Dietary Intake and Serum Level of Carotenoids in Lung Cancer Patients: A Case-Control Study

Asbaghi

Saedisomeolia

Hosseini

et al. 2015

Nutrition and Cancer

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“…The activation of the NF-κB transcription system is associated with harmful effect to bone health, and contributes to cancer development. The 10,10′-diapocarotene-10,10′-dial, which is the cleave products of lycopene by BCO2, was reported to inhibit NF-κB transcription system and to reduce the expression of NF-κB target genes [134]. Such process was mediated by the directly interaction of carotenoid derivatives with key kinases IKKβ and the p65 subunit.…”

Section: Carotenoids Bco2 and Mitochondrial Functionmentioning

confidence: 99%

Hypothalamic mitochondria in energy homeostasis and obesity

Guo¹,

Wu²,

Wang³

et al. 2016

Integr Mol Med

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Obesity, which is largely due to energy imbalance, has emerged as one of the most serious health issues in the world. The hypothalamus is the most important organ to regulate feeding behavior and energy expenditure through nutrient sensing and signal integration from central and peripheral pathways. As the main organelle to produce energy, mitochondria play a critical role in energy homeostasis from the organelle level. Besides providing a platform for the oxidation of fuel substrates, mitochondria are also involved in a variety of cell signaling pathways and modulate energy homeostasis through mitochondrial dynamics. Mitochondrial dysfunction may lead to obesity due to inadequate ATP production, oxidative stress, endoplasmic reticulum stress, and inflammation. β, β-carotene-9',10'-oxygenase2 (BCO2) is a mitochondrial enzyme that catalyzes the asymmetric cleavage of both provitamin A and non-provitamin A carotenoids. This enzyme is localized to the inner mitochondrial membrane, where the electron transport chain is located. Besides the enzymatic function, BCO2 is important for mitochondrial function and is genetically associated with interleukin-18. Moreover, BCO2 protein expression is suppressed in obese and diabetic mice. Given that the important role of BCO2 in mitochondrial structure and function, and the key position of the hypothalamus in energy balance, BCO2 may play a new role in maintaining metabolic homeostasis that has been overlooked before. The mutation of BCO2 might lead to the impairment of whole body energy homeostasis through hypothalamic mitochondrial dysfunction. Here we will be presenting the updates on hypothalamic mitochondria in cellular energy homeostasis and discussing the potential of BCO2 in regulation of hypothalamic mitochondria in health and obesity.

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