Maternal Iron Deficiency Alters Essential Fatty Acid and Eicosanoid Metabolism and Increases Locomotion in Adult Guinea Pig Offspring

Leblanc, Claude; Fiset, Sylvain; Surette, Marc E.; O’Brien, Huguette Turgeon

doi:10.3945/jn.109.106013

Cited by 24 publications

(30 citation statements)

References 62 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, the iron contents of the two diets in this study were relatively high. These ingredients were based on prior studies [24,25]. In these studies, the iron content of the control diet is 70–145 mg/kg diet, the iron content of the ID diet is 8.44–30 mg/kg diet.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

RETRACTED: Low Iron Diet Increases Susceptibility to Noise-Induced Hearing Loss in Young Rats

Hao

Yang

et al. 2016

Nutrients

View full text Add to dashboard Cite

We evaluated the role of iron deficiency (ID) without anemia on hearing function and cochlear pathophysiology of young rats before and after noise exposure. We used rats at developmental stages as an animal model to induce ID without anemia by dietary iron restriction. We have established this dietary restriction model in the rat that should enable us to study the effects of iron deficiency in the absence of severe anemia on hearing and ribbon synapses. Hearing function was measured on Postnatal Day (PND) 21 after induction of ID using auditory brainstem response (ABR). Then, the young rats were exposed to loud noise on PND 21. After noise exposure, hearing function was again measured. We observed the morphology of ribbon synapses, hair cells and spiral ganglion cells (SGCs), and assessed the expression of myosin VIIa, vesicular glutamate transporter 3 and prestin in the cochlea. ID without anemia did not elevate ABR threshold shifts, but reduced ABR wave I peak amplitude of young rats. At 70, 80, and 90 dB SPL, amplitudes of wave I (3.11 ± 0.96 µV, 3.52 ± 1.31 µV, and 4.37 ± 1.08 µV, respectively) in pups from the ID group were decreased compared to the control (5.92 ± 1.67 µV, 6.53 ± 1.70 µV, and 6.90 ± 1.76 µV, respectively) (p < 0.05). Moreover, ID without anemia did not impair the morphology hair cells and SGCs, but decreased the number of ribbon synapses. Before noise exposure, the mean number of ribbon synapses per inner hair cell (IHC) was significantly lower in the ID group (8.44 ± 1.21) compared to that seen in the control (13.08 ± 1.36) (p < 0.05). In addition, the numbers of ribbon synapses per IHC of young rats in the control (ID group) were 6.61 ± 1.59, 3.07 ± 0.83, 5.85 ± 1.63 and 12.25 ± 1.97 (3.75 ± 1.45, 2.03 ± 1.08, 3.81 ± 1.70 and 4.01 ± 1.65) at 1, 4, 7 and 14 days after noise exposure, respectively. Moreover, ABR thresholds at 4 and 8 kHz in young rats from the ID group were significantly elevated at 7 and 14 days after noise exposure compared to control (p < 0.05). The average number of young rat SGCs from the ID group were significantly decreased in the basal turn of the cochlea compared to the control (p < 0.05). Therefore, ID without anemia delayed the recovery from noise-induced hearing loss and ribbon synapses damage, increased SGCs loss, and upregulated prestin after noise exposure. Thus, the cochleae in rat pups with ID without anemia were potentially susceptible to loud noise exposure, and this deficit may be attributed to the reduction of ribbon synapses and SGCs.

show abstract

Section: Discussionmentioning

confidence: 99%

“…The other group (iron deficient group; n = 10) was fed an iron deficient diet (iron content: 25.27 ± 9.08 mg/kg diet). These ingredients were based on prior studies [24,25]. Table 1 showed the composition of experimental diets.…”

Section: Methodsmentioning

confidence: 99%

RETRACTED: Low Iron Diet Increases Susceptibility to Noise-Induced Hearing Loss in Young Rats

Hao

Yang

et al. 2016

Nutrients

View full text Add to dashboard Cite

show abstract

“…Moreover, these deficiencies may directly interact via Fe-dependent hepatic desaturases involved in the conversion of essential FA into LCPUFA and/ or via Fe-dependent cyclooxygenase involved in the synthesis of eicosanoids derived from LCPUFA (7,17,18). However, to our knowledge, there are no published data in the study of animal models on the consequences of concurrent ID and (n-3)FAD on brain development and cognitive functioning.…”

Section: Introductionmentioning

confidence: 77%

“…Fe is a cofactor for enzymes involved in cell division and the synthesis of neurotransmitters, myelin, and brain eicosanoids (4)(5)(6)(7)(8) and therefore plays a central role in neuronal growth, differentiation, and myelination (8,9). Most studies of ID in rats have examined the pre-and early postnatal periods; less is known about the effects of ID in the postweaning phase.…”

Section: Introductionmentioning

confidence: 98%

Combined Deficiency of Iron and (n-3) Fatty Acids in Male Rats Disrupts Brain Monoamine Metabolism and Produces Greater Memory Deficits Than Iron Deficiency or (n-3) Fatty Acid Deficiency Alone

Baumgartner

Smuts

Malan

et al. 2012

The Journal of Nutrition

View full text Add to dashboard Cite

Deficiencies of iron (Fe) (ID) and (n-3) fatty acids (FA) [(n-3)FAD] may impair brain development and function through shared mechanisms. However, little is known about the potential interactions between these 2 common deficiencies. We studied the effects of ID and (n-3)FAD, alone and in combination, on brain monoamine pathways (by measuring monoamines and related gene expression) and spatial working and reference memory (by Morris water maze testing). Using a 2 × 2 design, male rats were fed an ID, (n-3)FAD, ID+(n-3)FAD, or control diet for 5 wk postweaning (postnatal d 21-56) after (n-3)FAD had been induced over 2 generations. The (n-3)FAD and ID diets decreased brain (n-3) FA by 70-76% and Fe by 20-32%, respectively. ID and (n-3)FAD significantly increased dopamine (DA) concentrations in the olfactory bulb (OB) and striatum, with an additive 1- to 2-fold increase in ID+(n-3)FAD rats compared with controls (P < 0.05). ID decreased serotonin (5-HT) levels in OB, with a significant decrease in ID+(n-3)FAD rats. Furthermore, norepinephrine concentrations were increased 2-fold in the frontal cortex (FC) of (n-3)FAD rats (P < 0.05). Dopa decarboxylase was downregulated in the hippocampus of ID and ID+(n-3)FAD rats (fold-change = -1.33; P < 0.05). ID and (n-3)FAD significantly impaired working memory performance and the impairment positively correlated with DA concentrations in FC (r = 0.39; P = 0.026). Reference memory was impaired in the ID+(n-3)FAD rats (P < 0.05) and was negatively associated with 5-HT in FC (r = -0.42; P = 0.018). These results suggest that the combined deficiencies of Fe and (n-3) FA disrupt brain monoamine metabolism and produce greater deficits in reference memory than ID or (n-3)FAD alone.

show abstract

“…Neuronal iron deposition causes oxidative stress via the Fenton reaction, which might contribute to elevated oxidative stress observed in the AD brain [109]. Iron-induced oxidative stress has been shown to initiate several apoptotic signaling pathways in neurons [110], and damage proteins such as Ca 2+ -ATPase [111][112][113][114], glutamate transporter [115][116][117], apolipoprotein E [118,119], and Na + /K + -ATPase [111,114,120,121], as well as N-methyl-D-aspartate (NMDA) receptor [122][123][124], and lipids such as cholesterol [125][126][127], ceramides [128,129], and unsaturated fatty acids [130][131][132][133], as well as sphingomyelin [134,135]. Oxidative damage to proteins and lipids by iron can cause synaptic dysfunction and neuronal cell death [136].…”

Section: Ironmentioning

confidence: 99%

Biometals and Their Therapeutic Implications in Alzheimer's Disease

2015

View full text Add to dashboard Cite

No disease modifying therapy exists for Alzheimer's disease (AD). The growing burden of this disease to our society necessitates continued investment in drug development. Over the last decade, multiple phase 3 clinical trials testing drugs that were designed to target established disease mechanisms of AD have all failed to benefit patients. There is, therefore, a need for new treatment strategies. Changes to the transition metals, zinc, copper, and iron, in AD impact on the molecular mechanisms of disease, and targeting these metals might be an alternative approach to treat the disease. Here we review how metals feature in molecular mechanisms of AD, and we describe preclinical and clinical data that demonstrate the potential for metal-based drug therapy.

show abstract

Maternal Iron Deficiency Alters Essential Fatty Acid and Eicosanoid Metabolism and Increases Locomotion in Adult Guinea Pig Offspring

Cited by 24 publications

References 62 publications

RETRACTED: Low Iron Diet Increases Susceptibility to Noise-Induced Hearing Loss in Young Rats

RETRACTED: Low Iron Diet Increases Susceptibility to Noise-Induced Hearing Loss in Young Rats

Combined Deficiency of Iron and (n-3) Fatty Acids in Male Rats Disrupts Brain Monoamine Metabolism and Produces Greater Memory Deficits Than Iron Deficiency or (n-3) Fatty Acid Deficiency Alone

Biometals and Their Therapeutic Implications in Alzheimer's Disease

Contact Info

Product

Resources

About