| ObjectivesTo observe the effects of dietary iron contents and long-term exercise on thehematological iron status, liver non-heme-iron (NHI) contents, hippocampal NHI contents,hippocampal lipid peroxidation and hippocampal hydroxyl radical metabolism in the malerats, and to investigate the effects of dietary iron contents and long-term exercise on theperipheral and hippocampal iron status.MethodsNinety weaning male rats were assigned into three groups: a dietary iron deficiencygroup (12mg/kg), a dietary iron sufficiency group (45mg/kg) and a high dietary ironcontent group (1000mg/kg), and each group was further divided into an exercise groupand a sedentary group: exercise group with dietary iron deficiency (EL), sedentary groupwith dietary iron deficiency (SL), exercise group with dietary iron sufficiency (ES),sedentary group with dietary iron sufficiency (SS), exercise group with high dietary ironcontent (EH), sedentary group with high dietary iron content (SH). After one month offeeding with corresponding iron content diets, the rats in three exercise groups wereexposed to swimming exercise for three months (5d/week, one exercise session/d), andthe rats in the corresponding sedentary groups were treated approximately the same way as the exercised rats, except for swimming. Animals were fasted for24hours after the lastexercise regimen and then blood collection was taken from their vein under pentobarbitalanesthesia for analyzing blood hemoglobin (Hb), hematocrit (Hct), mean corpuscularvolume (MCV), mean corpuscular hemoglobin (MCH), red cell distribution (RDW),serum iron (SI) and total iron binding capacity (TIBC). The liver and hippocampus werequick-freezing in liquid nitrogen, and then stored atï¼80°C refrigerator, for thedetermination of the NHI in the liver and hippocampus, MDA, inhibition of hydroxylradical capacity and SOD in the hippocampus.Results1. The impact of dietary iron contents and long-term exercise on peripheral iron status inmale ratsDietary iron contents affected Hb, Hct, MCV, MCH, RDW, SI, TIBC, TS and NHI inthe liver (P<0.05), and that exercise affected RDW and TIBC (P<0.05).Compared to SS group, Hb, Hct, MCV, MCH, SI, TS and NHI in the liver weredecreased (P<0.05), TIBC and RDW were significantly increased (P<0.01) in SL group.MCV was decreased (P<0.05), NHI in the liver was significantly increased (P<0.01), Hb,Hct, MCH, RDW, SI, TIBC and TS had no difference (P>0.05) in SH group.Compared to ES group, Hb, Hct, MCV, MCH, SI, TS and NHI in the liver weredecreased (P<0.05), TIBC and RDW were significantly increased (P<0.01) in EL group.NHI in the liver was significantly increased (P<0.01), Hb, Hct, MCV, MCH, RDW, SI,TIBC and TS had no difference (P>0.05) in EH group.Compared to SL group, TS was decreased (P<0.05), TIBC was significantlyincreased (P<0.01), Hb, Hct, MCV, MCH, RDW, SI and NHI in the liver had nodifference (P>0.05) in EL group.Compared to SS group, RDW was increased (P<0.05), Hb, Hct, MCV, MCH, SI,TIBC, TS and NHI in the liver had no difference (P>0.05) in ES group.Compared to SH group, NHI in the liver was significantly decreased (P<0.01), RDWwas increased (P<0.05), Hb, Hct, MCV, MCH, SI, TIBC and TS had no difference(P>0.05) in EH group. 2. The impact of dietary iron contents and long-term exercise on hippocampal iron status,lipid peroxidation, hydroxyl radical metabolism and SOD in male ratsDietary iron contents affected inhibition of hydroxyl radical capacity and SOD in thehippocampus (P<0.05), and that exercise affected MDA and inhibition of hydroxyl radicalcapacity in the hippocampus (P<0.05).Compared to SS group, MDA and inhibition of hydroxyl radical capacity in thehippocampus were decreased (P<0.05), NHI and SOD in the hippocampus had nodifference (P>0.05) in SL group. The inhibition of hydroxyl radical capacity in thehippocampus were increased (P<0.05), NHI, MDA and SOD in the hippocampus had nodifference (P>0.05) in SH group.Compared to ES group, NHI and inhibition of hydroxyl radical capacity in thehippocampus were decreased (P<0.05), MDA and SOD in the hippocampus had nodifference (P>0.05) in EL group. Inhibition of hydroxyl radical capacity and SOD in thehippocampus were significantly increased (P<0.01), NHI and MDA in the hippocampushad no difference (P>0.05) in EH group.Compared to SL group, NHI and inhibition of hydroxyl radical capacity in thehippocampus were decreased (P<0.05), MDA in the hippocampus was significantlyincreased (P<0.01), SOD in the hippocampus had no difference (P>0.05) in EL group.Compared to SS group, NHI, MDA, inhibition of hydroxyl radical capacity and SODin the hippocampus had no difference (P>0.05) in ES group.Compared to SH group, NHI, MDA, inhibition of hydroxyl radical capacity andSOD in the hippocampus had no difference (P>0.05) in ES group.Conclusion1. Long-term dietary iron deficiency could lead nutritional iron deficiency, and decreasethe NHI content in the liver. The high dietary iron content may not significantlychange the hematological iron status, but increase the NHI in the liver contentsleading iron overload.2. In the case of low dietary iron content, long-term exercise could further decreaseserum iron status, but could not change the NHI content in the liver, suggesting that long-term exercise may have a mechanism to cope with the depletion of liver ironstorage under iron deficiency. In the case of sufficient dietary iron content, long-termexercise may increase RDW with a trend toward decrease of the NHI content in theliver (but not a significant difference). In the case of high dietary iron content,long-term exercise may decrease the NHI content in the liver so as to reduce the ironburden of the liver.3. Dietary iron contents and long-term exercise may not individually change the NHI inthe hippocampus. In the case of dietary iron deficiency, long-term exercise coulddecrease the NHI in the hippocampus. In the case of sufficient or high dietary ironcontent, long-term exercise may not significantly change the NHI in thehippocampus.4. Long-term dietary iron deficiency could increase hydroxyl radical level in thehippocampus, which could cause free radical damage to the hippocampus. In the caseof high dietary iron content, hydroxyl radical level and SOD increased, At this point,increasing dietary iron content moderately may be helpful for protecting thehippocampus from free radical damage. In the case of low dietary iron content,long-term exercise could increase hydroxyl radical level and lipid peroxidation in thehippocampus which may exacerbate peroxidation damage. In the case of sufficient orhigh dietary iron content, long-term exercise may have no significantly changes onthe NHI of the hippocampus as well as lipid peroxidation, hydroxyl radical level andSOD in the hippocampus. |
