The efficacy of early iron supplementation on postpartum depression, a randomized double-blind placebo-controlled trial.

PURPOSE: Evaluating early iron supplementation in non-anemic mothers with postpartum depression (PPD). METHODS: This randomized, double-blind, placebo-controlled trial evaluated 70 mothers with PPD. One week after delivery, the mothers were randomly allocated in the iron-treated (50 mg elemental iron/daily) and placebo-treated groups. After 6 weeks, the improvement of PPD symptoms was compared between the groups. RESULTS: Ferritin significantly increased in the iron-treated group (p < 0.001), but not in the placebo group (p = 0.09). After intervention, ferritin was higher in the iron-treated group (medians: 78.2 vs. 37 mg/dl, p = 0.01). The rate of iron deficiency significantly decreased in the iron-treated group (p = 0.009), but not in the placebo group (p = 0.4). After intervention, the rate of iron deficiency was higher in the placebo group (31.4 vs. 8.5 %, p = 0.01). The Edinburgh Postnatal Depression Scale (EPDS) score significantly decreased in the iron-treated group (p < 0.001), but not in the placebo group (p = 0.13). After intervention, the EPDS score was lower in the iron-treated group (medians 9 vs. 12, p = 0.01). The improvement rate for PPD was significantly higher in the iron-treated group (42.8 vs. 20 %, p = 0.03). After intervention, mothers with continued PPD had lower ferritin than the improved mothers (41.8 vs. 67 mg/dl, p = 0.03). Mothers with continued depression had higher rate of iron deficiency compared to the improved mothers (27.1 vs. 4.5 %, p = 0.02). CONCLUSIONS: Early iron supplementation in mothers with PPD significantly improves the iron stores and causes a significant improvement in PPD with a 42.8 % improvement rate during 6 weeks. Continued PPD might be related to the lower postpartum ferritin levels in untreated mothers.

Profiling the physiological and molecular response to sulfonamidic drug in Procambarus clarkii.

Sulfamethoxazole (SMZ) is one of the most widely employed sulfonamides. Because of the widespread use of SMZ, a considerable amount is indeed expected to be introduced into the environment. The cytotoxicity of SMZ relies mainly on arylhydroxylamine metabolites (S-NOH) of SMZ and it is associated with the production of reactive oxygen species (ROS). There is limited information about the toxic potential of SMZ at the cellular and molecular levels, especially in aquatic and/or non-target organisms. In the present study, the red swamp crayfish (Procambarus clarkii), being tolerant to extreme environmental conditions and resistant to disease, was used as a model organism to profile the molecular and physiological response to SMZ. Haemolymphatic-immunological parameters such as glucose serum levels and total haemocyte counts were altered; moreover, a significant increase in Hsp70 plasma levels was detected for the first time. Variations at the transcriptional level of proinflammatory genes (cyclooxygenase-1, COX 1, and cyclooxygenase-2, COX 2), antioxidant enzymes (glutathione-S-transferase, GST and manganese superoxide dismutase MnSOD), stress response and Fenton reaction inhibitor genes (heat-shock protein 70 HSP70, metallothionein, MT and ferritin, FT) were evaluated, and alterations in the canonical gene expression patterns emerged. Considering these results, specific mechanisms involved in maintaining physiological homeostasis and adaptation in response to perturbations are suggested.

Anti-anaemia efficacy of ß-lactoglobulin hydrolysate-iron complex on iron-deficient anaemic rats.

PURPOSE: The effects of orally administered ß-lactoglobulin hydrolysate-iron complex (ß-LGH-Fe) on haematological and biochemical parameters in anaemic rats were evaluated. Female weaning Sprague-Dawley rats were fed with iron-deficient diet to induce iron deficiency anaemia. After 6 weeks, the obtained anaemic rats were divided into five groups: iron deficiency control group (iron-deficient diet without ß-LGH-Fe complex supplementation, IDC); three groups supplemented with different dosages of ß-LGH-Fe complex (0.5 mg Fe/kg BW, iron-deficient diet with low ß-LGH-Fe, IDLFe; 2.0 mg Fe/kg BW, iron-deficient diet with medium ß-LGH-Fe, IDMF; 4.0 mg Fe/kg BW, iron-deficient diet with high ß-LGH-Fe, IDHFe); and ferrous sulphate-supplemented group at a dosage of 2.0 mg Fe/kg BW. RESULTS: ß-LGH-Fe complex could significantly improve hematocrit and haemoglobin decrease, and normalise the serum iron level, total iron-binding capacity and transferrin saturation of anaemic rats in a dose-dependent manner. Serum ferritin content and hepatic nonheme iron level were also increased. In addition, the antioxidant enzyme activities of superoxidase dismutase, catalase and glutathione peroxidase in both plasma and liver homogenate were improved. The production of malondialdehyde and pro-inflammatory cytokines (TNF-α and IL-6) decreased. CONCLUSIONS: It suggests that ß-LGH-Fe complex can ameliorate iron deficiency anaemia, which might make it a potential ingredient with anti-anaemia activity.