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Department of Biochemistry and Physiology of Nutrition, German Institute of Human Nutrition, D-14558 Bergholz-Rehbrücke, Germany
1To whom correspondence should be addressed.
The maximum dietary protein intake that does not cause adverse effects
in a healthy population is uncertain. We tested whether a high protein
intake enhances oxidative stress. Adult rats were adapted to different
casein-based diets containing either an adequate (13.8%; AP),
medium (25.7%; MP), or high (51.3%; HP) level of crude protein; a
fourth group received a HP diet but no
RRR-
-tocopherol acetate (HP-toc). After 15 wk of
feeding, plasma protein carbonyl concentration, liver lipid peroxide
levels [thiobarbituric acid-reacting substances (TBARS)], reduced
glutathione (GSH) status and leucine kinetics
([1-13C]leucine) were measured. Higher concentrations of
protein carbonyls and TBARS were found in rats fed the AP and the
HP-toc diets compared with those fed the MP and HP diets
(P < 0.05). GSH concentrations in plasma did not
differ but total blood GSH concentrations were significantly
(P < 0.05) lower in rats fed the HP-toc diet
compared with those fed the AP, MP and HP diets. Liver GSH
concentrations were significantly (P < 0.01) lower
in rats fed the AP diet compared with the other groups. Rates of
postabsorptive leucine oxidation (LeuOX) and flux (QLeu)
were positively correlated with the dietary protein level (for AP, MP,
and HP, respectively: LeuOX, 74.9 ± 28.5, 109 ± 35.2, 142.3
± 38.4 µmol/(kg · h); QLeu, 425 ± 102, 483
± 82, 505 ± 80 µmol/(kg · h). Only HP-toc resulted
in a significantly greater protein breakdown (PBLeu) and
QLeu. No difference was seen in nonoxidative leucine
disposal. Long-term intake of high protein diets did not increase
variables of oxidative stress, in contrast to our initial hypothesis.
An unexpected finding was that adequate protein feeding (AP) may in
fact induce oxidative stress.
KEY WORDS: rats high protein diets oxidative stress leucine flux vitamin E deficiency
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