Dose-Responsive Alteration in Hepatic Lipid Peroxidation and Retinol Metabolism with Increasing Dietary beta-Carotene in Iron Deficient Rats

2002 ◽  
Vol 72 (5) ◽  
pp. 321-328 ◽  
Author(s):  
Ryouko Ikeda ◽  
Mariko Uehara ◽  
Misao Takasaki ◽  
Hiroshige Chiba ◽  
Ritsuko Masuyama ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Rat Liver ◽  
Control Diet ◽  
Beta Carotene ◽  
Deficient Diet ◽  
Wistar Strain ◽  
Iron Deficient ◽  
Hepatic Lipid Peroxidation ◽  
Retinol Metabolism ◽  
Retinol Concentration

Phosphatidylcholine hydroperoxide (PCOOH) levels are increased in the iron-deficient rat liver. We investigated the antioxidative effect of dietary beta-carotene and altered retinol metabolism in iron-deficient rats. Experiment 1: Male Wistar-strain rats were divided into six groups and fed a control diet, an iron-deficient diet, and iron-deficient diets with four different levels of dietary beta-carotene. The PCOOH concentration in the iron-deficient rat liver was decreased by supplementation with dietary beta-carotene. However, the beta-carotene dose response was not related to antioxidative potency. Hepatic and plasma beta-carotene concentrations were increased by iron deficiency. The hepatic retinol concentration was increased while the plasma retinol concentration was decreased in iron-deficient rats. Experiment 2: Male Wistar-strain rats were divided into two groups, with one group receiving a control diet with beta-carotene and the other an iron-deficient diet with beta-carotene. Intestinal iron was decreased and intestinal beta-carotene was unchanged in iron-deficient rats. The intestinal beta-carotene conversion ratio and beta-carotene cleavage enzyme activity were decreased in iron-deficient rats. Dietary beta-carotene played the role of an antioxidant in hepatic lipid peroxidation in the iron-deficient state, but there was no dose dependency. Moreover, intestinal beta-carotene cleavage and hepatic retinol release appear to be altered in iron-deficient rats.

scholarly journals Carrageenan-induced granuloma and iron status in rats with dietary polyunsaturated fatty acid deficiency

1991 ◽  
Vol 65 (3) ◽  
pp. 497-503 ◽  
Author(s):  
T. Carbonell ◽  
M. P. Saiz ◽  
M. T. Mitjavila ◽  
P. Puig-Parellada ◽  
C. Cambon-Gros ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acid ◽  
Polyunsaturated Fatty Acid ◽  
Iron Status ◽  
Control Diet ◽  
Fe Deficiency ◽  
Prostaglandin E ◽  
Sprague Dawley ◽  
Deficient Diet ◽  
Dietary Polyunsaturated Fatty Acid

Sprague–Dawley rats were fed for 4 months on a control diet or a polyunsaturated-fatty-acid (PUFA)-deficient diet. The combined effects of iron overload (Fe dextran) or Fe deficiency (desferrioxamine) on carrageenan-induced granuloma were studied. PUFA deficiency induced changes in Fe metabolism, but no alterations in lipid peroxidation variables were observed. Inflammation implied an increase in lipid peroxidation, Fe storage and caeruloplasmin concentration, together with symptoms of anaemia. PUFA deficiency in inflamed rats gave rise to a lower inflammatory response (granuloma weight and prostaglandin E2concentration) and ethane exhalation. Fe overload potentiated inflammatory and lipid peroxidation processes, whereas Fe deficiency decreased them.

scholarly journals Magnesium and calcium deficiencies additively increase zinc concentrations and metallothionein expression in the rat liver

2012 ◽  
Vol 109 (3) ◽  
pp. 425-432 ◽  
Author(s):  
Megumi Kotani ◽  
Ki Hyun Kim ◽  
Natsumi Ishizaki ◽  
Masayuki Funaba ◽  
Tohru Matsui
Keyword(s):  
Rat Liver ◽  
Control Diet ◽  
Mrna Level ◽  
Male Rats ◽  
Mrna Levels ◽  
Deficient Diet ◽  
Mg Deficiency ◽  
Ca Deficiency ◽  
Zn Concentration ◽  
Dietary Treatments

Mg deficiency increases the concentration of Zn in the liver. We investigated the effect of Mg deficiency on the expression of Zn-regulating factors such as Zn transporters and metallothionein (MT) in the rat liver. Because Ca deficiency alleviates some of the effects of Mg deficiency, we also investigated the interactions associated with Ca and Mg deficiencies. Growing male rats were given a control diet, a Mg-deficient diet, a Ca-deficient diet and a Mg- and Ca-deficient diet for 3 weeks. Mg and Ca deficiencies additively increased the mRNA levels of MT-1 and MT-2, the MT protein concentration and the concentration of Zn in the liver. The hepatic mRNA level of Zip14 increased with Mg deficiency but not with Ca deficiency. The dietary treatments did not affect the mRNA levels of other Zn transporters such as Zip1, Zip5, ZnT1, ZnT5 and ZnT6 in the liver. Ca deficiency was found to decrease the amount of femoral Zn and increase serum Zn concentration. This did not occur in the case of Mg deficiency. These results suggest that Mg deficiency enhances hepatic Zn uptake by the up-regulation of Zip14 expression and increases hepatic Zn concentration, leading to the enhancement of MT expression. Ca deficiency causes a transfer of Zn from the bone to the liver, which increases hepatic Zn concentration and, in turn, up-regulates the expression of MT. Because Mg and Ca deficiencies increase hepatic Zn concentration and increase MT expression by different mechanisms, their effects are additive.

scholarly journals Haloperidol increases hepatic lipid peroxidation promoted by high-fat diet in rats

2020 ◽  
Vol 9 (2) ◽  
pp. e148922153
Author(s):  
Ilson Dias da Silveira ◽  
Daniel Henrique Roos ◽  
Andréia Caroline Fernandes Salgueiro ◽  
Vanderlei Folmer ◽  
João Batista Teixeira da Rocha ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Negative Correlation ◽  
High Fat Diet ◽  
Control Diet ◽  
Abdominal Fat ◽  
Fat Content ◽  
High Fat ◽  
Intracellular Magnesium ◽  
Hepatic Lipid ◽  
Hepatic Lipid Peroxidation

This study aimed to evaluate the effects of the treatment with haloperidol (HAL) associated with a high-fat diet (HF) on hepatic and renal damage, intracellular magnesium (Mg2+) levels, and abdominal fat content. Young male Wistar rats were fed with high-fat diet or control diet during 48 weeks and, at the 24-week, part of animals began to be co-treated with HAL (1 mg/Kg/day intramuscularly). After 4 weeks of the drug administration, the livers and kidneys were removed for analyses. The results showed that HF diet significantly increased lipid peroxidation in the hepatic tissue of treated animals, when compared to animals treated with control diet (P<0.05). Moreover, HF associated with HAL further increased the hepatic lipid peroxidation levels (P<0.05). In contrast, HF and/or HAL did not promote significant changes in renal lipid peroxidation levels. We also found a negative correlation between intracellular Mg2+ levels and abdominal fat content among all animals. In conclusion, the data presented suggest adverse interactions between HAL and HF on liver. Furthermore, the negative correlation between the intracellular Mg2+ levels and the abdominal fat accumulation suggest a possible involvement of Mg2+ in the metabolic syndrome development associated with a HF diet.

Dietary iron-deficient anemia induces a variety of metabolic changes and even apoptosis in rat liver: a DNA microarray study

2010 ◽  
Vol 42 (2) ◽  
pp. 149-156 ◽  
Author(s):  
Asuka Kamei ◽  
Yuki Watanabe ◽  
Tomoko Ishijima ◽  
Mariko Uehara ◽  
Soichi Arai ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Iron Deficiency ◽  
Dna Microarray ◽  
Global Analysis ◽  
Control Diet ◽  
Diet Group ◽  
Iron Level ◽  
Dietary Iron ◽  
Deficient Diet ◽  
Iron Deficient

Anemia can be induced by dietary iron deficiency, as well as by hemorrhagia. It may also be associated with changes in lipid metabolism. However, no global analysis detailing the consequences of iron deficiency in the liver has yet been conducted. Since the liver is a metabolically important organ and also a major iron-storing organ, we performed a comprehensive transcriptome analysis to determine the effects of iron deficiency on hepatic gene expression. Four-week-old rats were fed an iron-deficient diet, ∼3 ppm iron, ad libitum for 16 days. These rats were compared with similar rats pair-fed a control diet with a normal iron level, 48 ppm iron. The 16-day iron-deficient diet apparently induced anemia. On day 17, the rats were killed under anesthesia, and their livers were dissected for DNA microarray analysis. We identified 600 upregulated and 500 downregulated probe sets that characterized the iron-deficient diet group. In the upregulated probe sets, genes involved in cholesterol, amino acid, and glucose metabolism were significantly enriched, while genes related to lipid metabolism were significantly enriched in the downregulated probe sets. We also found that genes for caspases 3 and 12, which mediate endoplasmic reticulum (ER)-specific apoptosis, were upregulated in the iron-deficient group. Combined, these results suggest that iron deficiency exerts various influences, not only on nutrient metabolism but also on apoptosis, as a consequence of ER stress in the liver.

scholarly journals Pyridoxine Deficiency Exacerbates Neuronal Damage after Ischemia by Increasing Oxidative Stress and Reduces Proliferating Cells and Neuroblasts in the Gerbil Hippocampus

2020 ◽  
Vol 21 (15) ◽  
pp. 5551 ◽  
Author(s):  
Hyo Young Jung ◽  
Woosuk Kim ◽  
Kyu Ri Hahn ◽  
Min Soo Kang ◽  
Tae Hyeong Kim ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Neuronal Death ◽  
Neuronal Damage ◽  
Control Diet ◽  
Essential Element ◽  
Hippocampal Neurogenesis ◽  
Related Factor ◽  
Proliferating Cells ◽  
Deficient Diet ◽  
Pyridoxine Deficiency

We investigated the effects of pyridoxine deficiency on ischemic neuronal death in the hippocampus of gerbil (n = 5 per group). Serum pyridoxal 5′-phosphate levels were significantly decreased in Pyridoxine-deficient diet (PDD)-fed gerbils, while homocysteine levels were significantly increased in sham- and ischemia-operated gerbils. PDD-fed gerbil showed a reduction in neuronal nuclei (NeuN)-immunoreactive neurons in the medial part of the hippocampal CA1 region three days after. Reactive astrocytosis and microgliosis were found in PDD-fed gerbils, and transient ischemia caused the aggregation of activated microglia in the stratum pyramidale three days after ischemia. Lipid peroxidation was prominently increased in the hippocampus and was significantly higher in PDD-fed gerbils than in Control diet (CD)-fed gerbils after ischemia. In contrast, pyridoxine deficiency decreased the proliferating cells and neuroblasts in the dentate gyrus in sham- and ischemia-operated gerbils. Nuclear factor erythroid-2-related factor 2 (Nrf2) and brain-derived neurotrophic factor (BDNF) levels also significantly decreased in PDD-fed gerbils sham 24 h after ischemia. These results suggest that pyridoxine deficiency accelerates neuronal death by increasing serum homocysteine levels and lipid peroxidation, and by decreasing Nrf2 levels in the hippocampus. Additionally, it reduces the regenerated potentials in hippocampus by decreasing BDNF levels. Collectively, pyridoxine is an essential element in modulating cell death and hippocampal neurogenesis after ischemia.

scholarly journals Effect of choline deficiency on S-adenosylmethionine and methionine concentrations in rat liver

1989 ◽  
Vol 259 (3) ◽  
pp. 725-729 ◽  
Author(s):  
S H Zeisel ◽  
T Zola ◽  
K A daCosta ◽  
E A Pomfret
Keyword(s):  
Rat Liver ◽  
Control Diet ◽  
Choline Deficiency ◽  
Deficient Diet ◽  
Methyl Donor ◽  
C1 Metabolism ◽  
Consistent Manner

Choline and C1 metabolism pathways intersect at the formation of methionine from homocysteine. Hepatic S-adenosylmethionine (AdoMet) concentrations are decreased in animals ingesting diets deficient in choline, and it has been suggested that this occurs because the availability of methionine limits AdoMet synthesis. If the above hypothesis is correct, changes in hepatic AdoMet concentrations should relate in some consistent manner to changes in hepatic methionine concentrations. Rats were fed on a choline-deficient or control diet for 1-42 days. Hepatic choline concentrations in control animals were 105 nmol/g, and decreased to 50% of control after the first 7 days on the choline-deficient diet. Hepatic methionine concentrations decreased by less than 20%, with most of this decrease occurring between days 3 and 7 of choline deficiency. Hepatic AdoMet concentrations decreased by 25% during the first week, and continued to decrease (in total, by over 60%) during each subsequent week during which animals consumed a choline-deficient diet. Hepatic S-adenosylhomocysteine (AdoHcy) concentrations increased by 50% when animals consumed a choline-deficient diet. AdoHcy is formed when AdoMet is utilized as a methyl donor. In summary, choline deficiency can deplete hepatic stores of AdoMet under dietary conditions that only minimally decrease the availability of methionine within liver. Thus decreased availability of methionine may not have been the only mechanism whereby choline deficiency lowers hepatic AdoMet concentrations. We suggest that increased utilization of AdoMet might also have occurred.

Dietary Calcium Supplementation Suppresses Bone Formation in Magnesium-Deficient Rats

2006 ◽  
Vol 76 (3) ◽  
pp. 111-116 ◽  
Author(s):  
Hiroshi Matsuzaki ◽  
Misao Miwa
Keyword(s):  
Bone Formation ◽  
Calcium Supplementation ◽  
Control Diet ◽  
Formation Rate ◽  
Dietary Calcium ◽  
Mineral Apposition Rate ◽  
Control Group ◽  
Deficient Diet ◽  
Bone Formation Rate ◽  
Male Wistar Rats

The purpose of this study was to clarify the effects of dietary calcium (Ca) supplementation on bone metabolism of magnesium (Mg)-deficient rats. Male Wistar rats were randomized by weight into three groups, and fed a control diet (control group), a Mg-deficient diet (Mg- group) or a Mg-deficient diet having twice the control Ca concentrations (Mg-2Ca group) for 14 days. Trabecular bone volume was significantly lower in the Mg - and Mg-2Ca groups than in the control group. Trabecular number was also significantly lower in the Mg - and Mg-2Ca groups than in the control group. Mineralizing bone surface, mineral apposition rate (MAR), and surface referent bone formation rate (BFR/BS) were significantly lower in the Mg - and Mg-2Ca groups than in the control group. Furthermore, MAR and BFR/BS were significantly lower in the Mg-2Ca group than in the Mg - group. These results suggest that dietary Ca supplementation suppresses bone formation in Mg-deficient rats.

Troxerutin protects the isolated perfused rat liver from a possible lipid peroxidation by coumarin

Phytomedicine ◽  
2005 ◽  
Vol 12 (1-2) ◽  
pp. 52-61 ◽  
Author(s):  
B.S. Adam ◽  
R. Pentz ◽  
C.P. Siegers ◽  
O. Strubelt ◽  
M. Tegtmeier
Keyword(s):  
Lipid Peroxidation ◽  
Rat Liver ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver
Sign in / Sign up

Export Citation Format

Share Document