Effect of Zinc Status on Pubertal and Cognitive Functions in Male Offspring of Rats with Induced Zinc Deficiency During Gestation and Lactation
Biological Trace Element Research, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Basım Tarihi: 2026
- Doi Numarası: 10.1007/s12011-026-05338-5
- Dergi Adı: Biological Trace Element Research
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, Chemical Abstracts Core, EMBASE, MEDLINE, Natural Science Collection (ProQuest), Biological Science Database (ProQuest), Biomedical Reference Collection: Corporate Edition (EBSCO), Earth, Atmospheric, & Aquatic Science Collection (ProQuest), Health Research Premium Collection (ProQuest), Pharma Collection (ProQuest)
- Anahtar Kelimeler: Adolescent hormones, BDNF, Maternal zinc deficiency, Memory performance, Zinc supplementation
- İstanbul Medipol Üniversitesi Adresli: Evet
Özet
This study aimed to examine the consequences of maternal zinc deficiency (MZD) during pregnancy and lactation on spatial memory, puberty, and nutritional hormone levels in male rat offspring, and to assess whether zinc supplementation can mitigate these impairments. Twenty pregnant Wistar rats were fed either a zinc-deficient diet (2.8 mg/kg) or a standard zinc diet (130 mg/kg). Following weaning on postnatal day 21 (P21), the pups were allocated into four groups until the conclusion of the study on postnatal day 66 (P66): the Continued-deficiency group (Group 1), the Postweaning dietary-repletion group (Group 2), the Dietary repletion plus intraperitoneal zinc group (Group 3), and the Control group (Group 4). Cognitive performance was assessed using the Morris water maze. Gene expression levels in the hippocampus and hypothalamus (ZnT3, BDNF, NPY, GnRH, Kisspeptin, GATAD1) were determined via RT-qPCR, while serum hormone levels were measured using ELISA. The residual effects of maternal zinc deficiency (MZD) were isolated by comparing Group 2 (postweaning dietary-repletion group) and Group 4 (control group); despite postweaning dietary rescue, Group 2 failed to resolve the significant suppressions in hippocampal ZnT3 and BDNF, and hypothalamic kisspeptin gene expressions, demonstrating the long-lasting molecular footprint of early-life exposure. To evaluate the compounding impact of ongoing postnatal deficiency, we compared Group 1 (continued-deficiency group) with Group 2, revealing that continued postweaning deficiency further exacerbated spatial memory deficits and neuroendocrine suppression. Intraperitoneal zinc supplementation provided an additional therapeutic effect beyond standard diet alone (Group 3 vs. Group 2), successfully restoring behavioral and molecular parameters. Notably, this pharmacological intervention returned these levels back to control-like, physiological values (Group 3 vs. Group 4) without exceeding the physiological range.