Interactions in the postprandial appearance of beta-carotene and canthaxanthin in plasma triacylglycerol-rich lipoproteins in humans.

We investigated the plasma appearance of beta-carotene and canthaxanthin, an oxycarotenoid, in normolipidemic premenopausal women (n = 9) who ingested beta-carotene alone, canthaxanthin alone, and a combined dose. Blood samples were taken hourly for 12 h; additional blood samples were collected over 528 h. In a subset of the women (n = 5), plasma lipoproteins were separated into chylomicrons, very-low-density-lipoproteins (VLDL) subfractions, intermediate-density lipoproteins (IDLs), and low-density lipoproteins (LDLs). The appearance of beta-carotene in plasma was biphasic, with a minor peak at 5 h followed by a sustained peak at 24-48 h. The plasma appearance of canthaxanthin was monophasic, with a rapid increase to the final hourly measurement at 12 h and a steady decrease from the next measurement at 24 h. At 6 h, 23.4 +/- 2.9% of the increase in plasma canthaxanthin was associated with LDL, in contrast with 2.4 +/- 1.4% of the increase in plasma beta-carotene (P < 0.005). Ingestion of a combined dose of beta-carotene and canthaxanthin inhibited the appearance of canthaxanthin in plasma, chylomicrons, and each VLDL subfraction (P < 0.05), but did not significantly affect the rapid accumulation of canthaxanthin in LDL within 10 h. In contrast, ingestion of the combined dose did not significantly affect the appearance of beta-carotene in plasma or plasma lipoproteins. These findings suggest distinct mechanisms of incorporation into lipoproteins and specific interactions of beta-carotene and canthaxanthin during intestinal absorption in humans.

Carotenoids in human buccal mucosa cells after 4 wk of supplementation with tomato juice or lycopene supplements.

BACKGROUND: Lycopene has been identified as a phytochemical with potentially protective health benefits. OBJECTIVE: Our objective was to monitor lycopene changes in buccal mucosa cells (BMCs) in response to 3 vehicles for oral delivery of lycopene. DESIGN: Fifteen healthy subjects ingested lycopene-rich tomato juice, tomato oleoresin, lycopene beadlets (each containing 70-75 mg lycopene) and a placebo for 4 wk each in a randomized crossover design while consuming self-selected diets. A 6-wk washout period separated the treatment periods. BMCs were collected at baseline and after 4 wk of supplementation. RESULTS: Lycopene in BMCs increased significantly ( approximately 2-fold) after 4 wk of ingestion of oleoresin and of beadlets to 4.95 (P < 0.001) and 3.75 microg/g protein (P = 0.053), respectively, but was not significantly affected by tomato juice treatment. The placebo treatment produced a significant decrease in BMC lycopene concentrations (P = 0.018). We observed significant treatment differences between oleoresin and tomato juice, oleoresin and placebo, and beadlets and placebo. BMC concentrations of phytofluene and beta-carotene, which were present in small amounts in the lycopene-containing treatments, increased significantly with ingestion of these products. Strong correlations were found between plasma and BMC concentrations of lutein, beta-cryptoxanthin, alpha-carotene, and beta-carotene. In contrast, correlations between lycopene concentrations in plasma and in BMCs were weak and not significant for any treatment. CONCLUSIONS: The cellular content of lycopene and other tomato-related carotenoids with proposed beneficial health effects can be increased through prolonged supplementation.

Chronic ingestion of lycopene-rich tomato juice or lycopene supplements significantly increases plasma concentrations of lycopene and related tomato carotenoids in humans.

The bioavailability of lycopene from tomato juice and 2 dietary supplements, each containing 70-75 mg lycopene, was studied in 15 healthy volunteers in a randomized, crossover design. Subjects ingested lycopene-rich tomato juice, tomato oleoresin, lycopene beadlets, and a placebo for 4 wk each while consuming self-selected diets. Treatment periods were separated by 6-wk washout periods. Plasma lycopene concentrations, assessed at baseline and weekly throughout the treatment periods, were significantly higher during tomato juice, oleoresin, and lycopene beadlet ingestion than during placebo ingestion. Mean (+/-SEM) increases in plasma lycopene at week 4 of tomato juice, oleoresin, and lycopene beadlet ingestion were not significantly different: 0.24 +/- 0.07, 0.23 +/- 0.05, and 0.24 +/- 0.06 micromol/L, respectively. Plasma concentrations of phytofluene and phytoene, which were present in small amounts in tomato juice, oleoresin, and lycopene beadlets, increased significantly with ingestion of these 3 products. Beta-carotene, zeta-carotene, and 2,6-cyclolycopene-1,5-diol (a metabolite of lycopene)--also present in tomato juice and supplements--were significantly increased with consumption of the tomato juice and lycopene beadlets, but not with oleoresin consumption. A marked increase in plasma concentrations of an unknown compound was observed; it was detected in trace amounts in tomato juice, oleoresin, and lycopene beadlets, and had a maximum absorbance at 448 nm and a molecular weight of 556. Concentrations of plasma lycopene and other carotenoids with potential for enhancing human health can be increased by ingestion of realistic amounts of tomato juice. Lycopene appears to be equally bioavailable from tomato juice and the supplements used in this study.

POLG1 manifestations in childhood.

OBJECTIVE: Mitochondrial DNA polymerase γ (POLG1) mutations in children often manifest as Alpers syndrome, whereas in adults, a common manifestation is mitochondrial recessive ataxia syndrome (MIRAS) with severe epilepsy. Because some patients with MIRAS have presented with ataxia or epilepsy already in childhood, we searched for POLG1 mutations in neurologic manifestations in childhood. METHODS: We investigated POLG1 in 136 children, all clinically suspected to have mitochondrial disease, with one or more of the following: ataxia, axonal neuropathy, severe epilepsy without known epilepsy syndrome, epileptic encephalopathy, encephalohepatopathy, or neuropathologically verified Alpers syndrome. RESULTS: Seven patients had POLG1 mutations, and all of them had severe encephalopathy with intractable epilepsy. Four patients had died after exposure to sodium valproate. Brain MRI showed parieto-occipital or thalamic hyperintense lesions, white matter abnormality, and atrophy. Muscle histology and mitochondrial biochemistry results were normal in all. CONCLUSIONS: POLG1 analysis should belong to the first-line DNA diagnostic tests for children with an encephalitis-like presentation evolving into epileptic encephalopathy with liver involvement (Alpers syndrome), even if brain MRI and morphology, respiratory chain activities, and the amount of mitochondrial DNA in the skeletal muscle are normal. POLG1 analysis should precede valproate therapy in pediatric patients with a typical phenotype. However, POLG1 is not a common cause of isolated epilepsy or ataxia in childhood.