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      Effect of different cooking methods on the content of vitamins and true retention in selected vegetables

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          Abstract

          <p class="first" id="Par1">This study evaluated the effect of different cooking methods including blanching, boiling, microwaving and steaming on the content of vitamins in vegetables. True retention was estimated using the yield expressed as a ratio of the weight of the cooked sample to the weight of the raw sample. The retention of vitamin C ranged from 0.0 to 91.1% for all cooked samples. Generally, higher retention of vitamin C was observed after microwaving with the lowest retention recorded after boiling. Cooked vegetables were occasionally higher contents of fat-soluble vitamins, including α-tocopherol and β-carotene, than that of their fresh counterparts, but it depends on the type of vegetables. Microwave cooking caused the greatest loss of vitamin K in crown daisy and mallow; in contrast, it caused the least loss of vitamin K in spinach and chard. Cooking may cause changes to the contents of vitamins, but it depends on vegetables and cooking processes. </p>

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           -Tocopherol and beta-Carotene Supplements and Lung Cancer Incidence in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study: Effects of Base-line Characteristics and Study Compliance

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            β-Carotene and α-tocopherol are synergistic antioxidants

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              Influence of vitamin C and vitamin E on redox signaling: Implications for exercise adaptations.

              The exogenous antioxidants vitamin C (ascorbate) and vitamin E (α-tocopherol) often blunt favorable cell signaling responses to exercise, suggesting that redox signaling contributes to exercise adaptations. Current theories posit that this antioxidant paradigm interferes with redox signaling by attenuating exercise-induced reactive oxygen species (ROS) and reactive nitrogen species (RNS) generation. The well-documented in vitro antioxidant actions of ascorbate and α-tocopherol and characterization of the type and source of the ROS/RNS produced during exercise theoretically enable identification of redox-dependent mechanisms responsible for the blunting of favorable cell signaling responses to exercise. This review aimed to apply this reasoning to determine how the aforementioned antioxidants might attenuate exercise-induced ROS/RNS production. The principal outcomes of this analysis are (1) neither antioxidant is likely to attenuate nitric oxide signaling either directly (reaction with nitric oxide) or indirectly (reaction with derivatives, e.g., peroxynitrite); (2) neither antioxidant reacts appreciably with hydrogen peroxide, a key effector of redox signaling; (3) ascorbate but not α-tocopherol has the capacity to attenuate exercise-induced superoxide generation; and (4) alternate mechanisms, namely pro-oxidant side reactions and/or reduction of bioactive oxidized macromolecule adducts, are unlikely to interfere with exercise-induced redox signaling. Out of all the possibilities considered, ascorbate-mediated suppression of superoxide generation with attendant implications for hydrogen peroxide signaling is arguably the most cogent explanation for blunting of favorable cell signaling responses to exercise. However, this mechanism is dependent on ascorbate accumulating at sites rich in NADPH oxidases, principal contributors to contraction-mediated superoxide generation, and outcompeting nitric oxide and superoxide dismutase isoforms. The major conclusions of this review are: (1) direct evidence for interference of ascorbate and α-tocopherol with exercise-induced ROS/RNS production is lacking; (2) theoretical analysis reveals that both antioxidants are unlikely to have a major impact on exercise-induced redox signaling; and (3) it is worth considering alternate redox-independent mechanisms.
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                Author and article information

                Journal
                Food Science and Biotechnology
                Food Sci Biotechnol
                Springer Science and Business Media LLC
                1226-7708
                2092-6456
                December 12 2017
                Article
                10.1007/s10068-017-0281-1
                6049644
                30263756
                3055abad-0094-472a-b4ec-a31c9072d0f5
                © 2017

                http://www.springer.com/tdm

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