Long-term high protein intake does not increase oxidative stress in rats

The maximum dietary protein intake that does not cause adverse effects in a healthy population is uncertain, We tested whether a high protein intake e nhances oxidative stress. Adult rats were adapted to different casein-based diets containing either an adequate (13.8%; AP), medium (25.7%; MP), or hi gh (51.3%; HP) level of crude protein; a fourth group received a HP diet bu t no RRR-alpha -tocopherol acetate (HP-toc). After 15 wk of feeding, plasma protein carbonyl concentration, liver lipid peroxide levels [thiobarbituri c acid-reacting substances (TBARS)], reduced glutathione (GSH) status and l eucine kinetics ([1-C-13]leucine) were measured. Higher concentrations of p rotein carbonyls and TEARS were found in rats fed the AP and the HP-toc die ts compared with those fed the MP and HP diets (P < 0.05). GSH concentratio ns in plasma did nor differ but total blood GSH concentrations were signifi cantly (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 IP < 0.01) lower in rats fed the AP diet compared with the other groups. Rates o f posrabsorptive leucine oxidation (LeuOX) and flux (Q(Leu)) were positivel y correlated with the dietary protein level (for AP, MP, and HP, respective ly: LeuOX, 74.9 +/- 28.5, 109 +/- 35.2, 142.3 +/- 38.4 <mu>mol/(kg(.)h); Q( Leu) 425 +/- 102, 483 +/- 82, 505 +/- 80 mu mol/(kg(.)h). Only HP-toc resul ted in a significantly greater protein breakdown (PBLeu) and Q(Leu). No dif ference 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.