Full-text resources of CEJSH and other databases are now available in the new Library of Science.
Visit https://bibliotekanauki.pl

Results found: 3

first rewind previous Page / 1 next fast forward last

Search results

Search:
in the keywords:  β-carotene
help Sort By:

help Limit search:
first rewind previous Page / 1 next fast forward last
1
100%
EN
High doses of synthetic antioxidative vitamins: A, E, C and β-carotene are often used on long-term basis in numerous preventive and therapeutic medical applications. Instead of expected health effects, the use of those vitamins may however lead to cases of hypervitaminosis and even to intoxication. The article points out main principles of safety which are to be observed during supplementation with antioxidative vitamins. Toxic effects resulting from erroneous administration of high doses of those substances on organs and systems of the organism are also discussed. Attention is drawn to interactions of antioxidative vitamins with concomitantly used drugs, as well as intensification of adverse effects caused by various exogenous chemical factors. Moreover, the article presents the evaluation of supplementation with these vitamins, which was performed in large studies.
EN
Long-term exposure to cadmium (Cd) leads to the development of a number of conditions associated with liver and kidney damage, reproductive and cardiovascular disorders, in addition to visual impairment, blindness and hearing loss, among others. Cadmium has been classified as a human carcinogen by the International Agency for Research on Cancer. The toxicity of Cd is related to its pro-oxidant properties and the associated increase in oxidative stress. Antioxidant ingredients may be helpful in preventing the adverse effects of Cd. The effect of well-known antioxidant vitamins (E, C, A and β-carotene) in the prevention of Cd-induced toxicity is presented in this study. Numerous studies in animal models have shown that the effects of vitamins: E, C, A, and β-carotene were effective in reducing Cd concentrations in organs and tissues and reduced Cd-induced changes in liver, kidney, and reproductive, circulatory, nervous, immune, and respiratory systems. In contrast, the limited number of human studies does not allow to accurately determine the role of these nutrients in reducing Cd-induced toxicity, indicating the need for further studies clarifying the role of antioxidant vitamins in reducing Cd-induced toxicity. However, it seems reasonable to promote the consumption of natural food products that are sources of antioxidant vitamins in groups of people with occupational and environmental exposure to Cd.
PL
Wstęp: Ponieważ ołów wywołuje stres oksydacyjny, przypuszcza się, że antyoksydanty mogą mieć zastosowanie w leczeniu zatrucia tym metalem. Celem niniejszej pracy było zbadanie, czy podawanie β-karotenu redukuje stres oksydacyjny oraz obniża stężenie homocysteiny u pracowników narażonych na ołów. Materiał i metody: Grupę badaną stanowili zdrowi pracownicy płci męskiej podzieleni na 2 podgrupy (średnie stężenie ołowiu we krwi: ok. 44 μg/dl). W pierwszej (N = 49, grupa porównawcza) nie stosowano żadnego leczenia, a drugiej podawano β-karoten w dawce 10 mg na dzień przez 12 tygodni. Analiza biochemiczna objęła markery narażenia na ołów i marker stresu oksydacyjnego - dialdehyd malonowy (malondialdehyde - MDA). Ponadto zbadano stężenie homocysteiny (homocysteine - Hcy), grup tiolowych oraz aktywność dysmutazy ponadtlenkowej (superoxide dismutase - SOD) i jej izoenzymu EC-SOD. Wyniki: Po suplementacji w grupie leczonej zaobserwowano obniżenie się stężenia MDA w porównaniu z wartościami wyjściowymi oraz z wynikami w grupie porównawczej. Obniżeniu uległo także stężenie Hcy w porównaniu z wynikami uzyskanymi dla grupy porównawczej. Z kolei stężenie grup tiolowych oraz aktywność SOD uległy zwiększeniu w porównaniu z grupą porównawczą, a w przypadku SOD i EC-SOD także w porównaniu z wartościami wyjściowymi. Wnioski: Wyniki niniejszego badania sugerują, że podawanie β-karotenu w zatruciu ołowiem może przynieść korzyści, takie jak zmniejszenie stresu oksydacyjnego, mierzonego pośrednio jako stężenie MDA, lub obniżenie stężenia aterogennej homocysteiny. Med. Pr. 2014;65(3):309–316
EN
Background: Oxidative stress is involved in lead toxicity. This suggests that some antioxidants may play a role in the treatment of lead poisoning. In the light of this, the aim of the study was to determine whether β-carotene administration reduces oxidative stress and homocysteine level in workers chronically exposed to lead. Material and Methods: The exposed population included healthy male workers exposed to lead who were randomly divided into 2 groups (mean blood lead level ca. 44 μg/dl). Workers in the 1st group (N = 49, reference group) had no antioxidants, drugs, vitamins or dietary supplements administered, while workers in the 2nd group (N = 33) had β-carotene administered in a dose of 10 mg per day for 12 weeks. Biochemical analysis included markers of lead-exposure and the level of malondialdehyde (MDA), an oxidative stress biomarker. We also measured the level of homocysteine (Hcy) and thiol groups as well as the activity of superoxide dismutase (SOD) and its isoenzyme EC-SOD in serum. Results: After supplementation, the level of MDA significantly decreased, compared to baseline, by 16%, and to the reference group. When compared to the reference group, Hcy level was also significantly decreased. However, the level of thiol groups was significantly higher after supplementation with β-carotene compared to the reference group. Analogically, the activity of SOD and EC-SOD was significantly higher compared to the baseline and to the reference group. Conclusions: Despite some controversies over antioxidant properties of β-carotene, our results indicate that its antioxidant action could provide some beneficial effects in lead poisoning independent of chelation. Med Pr 2014;65(3):309–316
first rewind previous Page / 1 next fast forward last
JavaScript is turned off in your web browser. Turn it on to take full advantage of this site, then refresh the page.