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beta-Carotene Degradation Products - Formation, Toxicity and Prevention of Toxicity

机译：β-胡萝卜素降解产物-形成，毒性和毒性预防

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Carotenoids are widely used as important micronutrients in food. Furthermore, carotenoid supplementation has been used in the treatment of diseases associated with oxidative stress such as various types of cancer, inflammatory diseases or cystic fibrosis. However, in some clinical studies harmful effects have been observed, e.g. a higher incidence of lung cancer in individuals exposed to extraordinary oxidative stress. The causal mechanisms of harmful effects are still unclear. Carotenoid breakdown products (CBPs) including highly reactive aldehydes and epoxides are formed during oxidative attacks in the course of antioxidative action. We investigated the formation of CBPs by stimulated neutrophils (and at further conditions), tested the hypothesisthat CBPs may exert mito-chondriotoxicity and tried to prevent toxicity in the presence of members of the antioxidative network. Stimulated neutrophils are able to degrade beta-carotene and to generate a number of CBPs. Concerning mitochondriotoxicity, we found that CBPs strongly inhibit state 3 respiration of rat liver mitochondria at concentrations between 0.5 and 20 mu M. This was true for retinal, beta-ionone, and for mixtures of cleavage/breakdown products. The inhibition of mitochondrial respiration was accompanied by a reduction in protein sulfhydryl content, decreasing GSH levels and redox state, and elevated accumulation of malondialdehyde. Changes in mitochondrial membrane potential favor functional deterioration in the adenine nucleotide translocator as a sensitive target. The presence of additional antioxidants such as a-tocopherol, ascorbic acid, N-acetyl-cysteine or others could mitigate mitochondriotoxicity. The findings reflect a basic mechanism of increasing the risk of cancer induced by carotenoid degradation products.
机译：类胡萝卜素被广泛用作食品中的重要微量营养素。此外，类胡萝卜素补充已用于治疗与氧化应激有关的疾病，例如各种类型的癌症，炎性疾病或囊性纤维化。然而，在一些临床研究中，已经观察到有害作用，例如。暴露于异常氧化应激的个体中肺癌的发病率更高。有害影响的因果机制仍不清楚。包括高反应性醛和环氧化物在内的类胡萝卜素分解产物（CBP）在抗氧化作用过程中的氧化侵蚀过程中形成。我们调查了受刺激的中性粒细胞（以及在其他条件下）形成的CBP，测试了CBP可能具有线粒体毒性的假设，并试图在存在抗氧化网络的成员的情况下防止毒性。受刺激的嗜中性粒细胞能够降解β-胡萝卜素并产生许多CBP。关于线粒体毒性，我们发现CBP在0.5至20μM的浓度下能强烈抑制大鼠肝线粒体的3状态呼吸。这对于视网膜，β-紫罗兰酮以及裂解/分解产物的混合物都是如此。线粒体呼吸的抑制伴随着蛋白质巯基含量的减少，GSH水平和氧化还原状态的降低以及丙二醛积累的增加。线粒体膜电位的变化有利于腺嘌呤核苷酸转运蛋白作为敏感靶标的功能恶化。其他抗氧化剂如α-生育酚，抗坏血酸，N-乙酰基半胱氨酸或其他抗氧化剂的存在可以减轻线粒体毒性。这些发现反映了增加类胡萝卜素降解产物诱发癌症风险的基本机制。

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