Biochemical aspects

         The metabolism of L(+)-malic acid is well understood, but little
    is known about the fate of D(-)-malic acid in the body. It has been
    suggested that L(+)-malic acid is more easily oxidized in the animal
    body (Pohl, 1896) and of parenterally administered DL-malic acid in
    rabbits and dogs only D(-)-malic acid was recovered in the urine
    (Tomita, 1921). Incubation of DL-malic acid with muscle enzyme
    preparations removes the L(+)-isomer preferentially (Dakin, 1922).
    Rabbits were injected with 1.7 or 2.0 g L(+)-malic acid and 1, 1.5 and
    3 g DL-malic acid. The L(+)-isomer was practically non-toxic, having a
    negligible effect on rate or over-all renal output of
    phenolsulfonphthalein and no effect on non-protein nitrogen and
    chloride level of the blood. The DL-isomer produced a reduction in the
    excretion rate and total output of the phthalein dye and a rise in
    non-protein nitrogen. Neither forms altered the blood creatinine level
    (Rose, 1925) The addition of DL-malic, acid to diets poor in
    carbohydrate led to an increase of glycogen in the liver of rats
    (Ponsford & Smedley-MacLean, 1932).

         Malic acid is an intermediate in the Krebs cycle.

Short-term studies

         A rabbit was killed after subcutaneous injections of DL-malic
    acid of 3 and 5 g on successive days and 1.5 g after omitting 1 day.
    Renal histology revealed small areas of cortical haemorrhages, some
    tubular epithelial degeneration and scattered glomerular obliteration
    (Rose, 1925).

    Long-term studies

         No studies in animals are available. Foods containing malic acid
    have been consumed by man for centuries without any apparent adverse
    effects. The daily human consumption of malic acid from vegetables,
    fruits and their juices is calculated to be in the order of 1.5 to 3 g
    (Hartman & Hillig, 1934).