<Emphasis Type="Italic">Selenium</Emphasis>-<Emphasis Type="Italic">Rich Yeast</Emphasis> protects against aluminum-induced peroxidation of lipide and inflammation in mice liver

To investigate the effect of Selenium Rich Yeast (SeY) on hepatotoxicity of Aluminium (Al), SeY (0.1 mg/kg) was orally administrated to aluminium-exposed mice (10 mg/kg) for 28 days. The risk of oxidative stress was assessed by detecting the total antioxidant capacity (T-AOC), catalase activity, H₂O₂ content, and mRNA levels of the Keap1/Nrf-2/HO-1 pathway. Inflammatory reactions were assessed by detecting the mRNA levels of inflammatory biomarkers. Our results showed that SeY protected against the liver histological changes induce by Al. The body weight gain of mice treated with SeY?+ Al restore to normal compare with mice exposed to Al alone. Al treatment significantly decreased the activities of antioxidant enzymes, reduced T-AOC levels, and up-regulated the mRNA level of Nrf2 and HO-1, thereby ultimately leading to peroxidation. SeY shown a significant protective effect against oxidative stress caused by Al. In addition, Al exposure induced inflammatory responses in rat liver by promoting the release of inflammatory cytokines (TNF-a, NF-kB, TNF-R1, IL-1, IL-6, and COX-2). SeY protected against changes in liver by regulating the mRNA expression levels of inflammatory factors. These results suggested that Se protected the liver from the Al-induced hepatotoxicity by regulating the mRNA level of Keap1/Nrf2/HO-1, and inhibited inflammatory responses by down-regulating the expression level of inflammatory cytokine.     

Neuroprotective Effects of Poly(ADP-ribose)polymerase Inhibitor Olaparib in Transient Cerebral Ischemia

Olaparib was the first poly(ADP-ribose)polymerase inhibitor approved by Food and Drug Administration for oncology treatment. However, its neuroprotective effects have not been elucidated. This study aimed to evaluate the effects of olaparib in transient cerebral ischemia. A mouse model of transient middle cerebral artery occlusion was used. Reperfusion was performed at 2 h after ischemia. Different doses of olaparib (1, 3, 5, 10 and 25 mg/kg) were administered intraperitoneally immediately after reperfusion. Twenty-four hours after ischemia, the neurological score was assessed, and grip and string tests were performed to evaluate the behavioral deficits in the mice. Cresyl violet staining was used to assess cerebral edema and the lesion volume. Immunohistochemistry was performed to evaluate the expression of blood–brain barrier proteins collagen IV and claudin-5, as well as extravasation of IgG. Ischemia induced a neurological deficit, which was significantly ameliorated by olaparib at 3 and 5 mg/kg. However, this neuroprotective effect was not observed in mice treated with either low-dose or high-dose olaparib. Both 3 and 5 mg/kg olaparib markedly reduced cerebral infarction volume, but not cerebral edema. The expression of collagen IV decreased after cerebral ischemia, which was improved by olaparib at 3 and 5 mg/kg. These results were confirmed by the reduction of IgG extravasation with olaparib. Olaparib showed clear neuroprotective effects in transient ischemic mice mainly through the reduction of cerebral infarction and blood–brain barrier damage.     

Effects of Lithium and Lamotrigine on Oxidative–Nitrosative Stress and Spatial Learning Deficit After Global Cerebral Ischemia

Lithium (Li) and lamotrigine (LTG) have neuroprotective properties. However, the exact therapeutic mechanisms of these drugs have not been well understood. We investigated the antioxidant properties of Li (40 and 80 mg/kg/day) and LTG (20 and 40 mg/kg/day) in a rat model of global cerebral ischemia based on permanent bilateral occlusion of the common carotid arteries (BCAO). Nitric oxide (NO), malondialdehyde (MDA), glutathione (GSH), glutathione reductase (GSH-R), catalase (CAT) and superoxide dismutase (SOD) levels were measured as an indicator of oxidative–nitrosative stress in both prefrontal cortex (PFC) and hippocampus after 28 days of treatment. The spatial learning disability was also assessed at the end of the study by Morris water maze (MWM) test. All oxidative–nitrosative parameters were found to be higher in the groups under treatment than in sham. Both drugs caused a decrease in PFC NO and MDA elevation, meanwhile the increase in GSH, GSH-R, CAT and SOD levels was significantly more evident in treated groups. We also found higher PFC GSH-R and hippocampal SOD levels in BCAO + Li (80 mg/day) treated group when compared with BCAO + LTG 40 mg/day. MWM test data showed a similar increase in spatial learning ability in all groups under treatment. We found no other statistical difference in comparison of treated groups with different dosages. Our findings suggested that Li and LTG treatments may decrease spatial learning memory deficits accompanied by lower oxidative–nitrosative stress in global cerebral ischemia. Both drugs may have potential benefits for the treatment of vascular dementia in clinical practice.     

Effect of Selenium from Selenium-Enriched Kale Sprout Versus Other Selenium Sources on Productivity and Selenium Concentrations in Egg and Tissue of Laying Hens

A 6-week trial was conducted to compare the effect of selenium (Se) from hydroponically produced Se-enriched kale sprout (HPSeKS), sodium selenite (SS), and Se-enriched yeast (SeY) in laying hens. A total of 144 40-week-old hens were randomly divided into four groups, according to a completely randomized design. Each group consisted of four replicates with nine hens per replicate. The dietary treatments were T1 (basal diet) and T2, T3, and T4 (basal diets supplemented with 0.30 mg Se/kg from SS, SeY, and HPSeKS, respectively). Results showed that Se supplement did not affect (p > 0.05) productivity and egg quality. Hens fed Se from HPSeKS and SeY exhibited higher (p < 0.05) Se bioavailability than hens fed Se from SS. Whole egg Se concentration of hens fed Se from HPSeKS was similar (p > 0.05) to that of hens fed Se from SeY, but higher (p < 0.05) than that of hens fed Se from SS. However, the breast muscle and heart tissue Se concentrations of hens fed Se from SS, SeY, and HPSeKS were not different (p > 0.05). The results of this trial demonstrated that Se from HPSeKS and SeY was more efficient than Se from SS on Se bioavailability and whole egg Se concentration in laying hens.     

Zinc, a Neuroprotective Agent Against Aluminum-induced Oxidative DNA Injury

Aluminum (Al) has been considered as one of the most abundant elements and comprises nearly 8 % of the Earth's crust. Despite of its immense presence, studies regarding the molecular basis of its interaction with the physiological system are rather sparse. On the other hand, zinc (Zn), an essential micronutrient, has been regarded as the second most important metal for brain functioning. The objective of the present study was to investigate the protective potential of Zn, if any, during Al-induced detrimental effects on DNA, tritiated thymidine uptake as well as expression of stress marker genes and proteins in rat brain. Male Sprague–Dawley rats weighing 140–160 g were divided into four different groups viz.: normal control, Al treated (100 mg/kg b wt/day via oral gavage), Zn treated (227 mg/l in drinking water), and combined Al and Zn treated. All the treatments were carried out for a total duration of 8 weeks. Agarose gel electrophoresis revealed DNA laddering pattern and comets in the rat brain following Al treatment, which however, were attenuated upon Zn treatment. Further, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-positive cells, number of apoptotic brain cells, and uptake of tritiated thymidine were increased after Al treatment but were decreased upon Zn supplementation. Western blot and mRNA expressions of p53 and nuclear factor κB (NF-κB) were also found to be significantly elevated after Al treatment, which however, were reversed following Zn treatment. Hence, Zn shall prove to be an effective agent in mitigating the detrimental effects caused by Al in the rat brain.     

Involvement of putrescine and nitric oxide in aluminum tolerance by modulating citrate secretion from roots of red kidney bean

Background and Aims

Polyamines and nitric oxide (NO) are two important molecules modulating numerous environment stresses in plants. This study was to investigate the roles of polyamines and NO in aluminum (Al) tolerance in red kidney bean.

Methods

The interaction between putrescine (Put) and NO under Al stress was examined. NO donor and scavenger were used to further examine the role of NO in Al-induced citrate secretion from roots by high performance liquid chromatography.

Results

Al stress caused increase of endogenous free Put, and exogenous Put alleviated Al-induced inhibition of root elongation and Al accumulation. In addition, Put induced NO production and nitrate reductase (NR) activity under Al stress. Al- and Put-induced NO production could be reversed by NR inhibitor. Furthermore, Al stress stimulated citrate secretion from roots, and this response was stimulated by NO donor, whereas NO scavenger inhibited Al-induced citrate secretion from roots. Concomitantly, NO donor reduced Al accumulation in root apexes, while NO scavenger further enhanced Al accumulation. Al-induced inhibition of root growth was significantly improved by exogenous citrate treatment.

Conclusions

Put and NO enhanced Al tolerance by modulating citrate secretion from roots, and NO may act downstream of Put in red kidney bean under Al stress.     

Influence of Different Amounts and Sources of Selenium Supplementation on Performance, Some Blood Parameters, and Nutrient Digestibility in Lambs

Two trials were conducted in a 2?×?2?+?1 factorial arrangement based on a completely randomized design to evaluate the effects of different sources of selenium (Se) on performance, blood metabolites, and nutrient digestibility in male lambs on a barley-based diet. The first trial lasted for 70 days and consisted of 30 lambs (35.6?±?2.6 kg mean body weight, about 4–5 months of age) which were randomly allotted to five treatments including: (1) basal diet (containing 0.06 mg Se/kg DM; control) without supplementary Se, (2) basal diet?+?0.20 mg/kg Se as sodium selenite (SeS 0.20), (3) basal diet?+?0.40 mg/kg Se as sodium selenite (SeS 0.40), (4) basal diet?+?0.20 mg/kg Se as selenium yeast (SeY 0.20), and (5) basal diet?+?0.40 mg/kg Se as selenium yeast (SeY 0.40). For the second trial, four lambs from each group of experiment 1 were randomly allocated to individual metabolic cages for 14 days to measure the effects of dietary Se on nutrient digestibility. The results revealed that there were no significant differences for average daily gain, average daily feed intake, feed/gain ratio, hematological parameters (packed cell volume, red blood cell, white blood cell, and hemoglobin values), serum total protein, albumin, globulin, aspartate amino transferase, alkaline phosphatase, and creatine phosphokinase due to supplementation of different amounts and sources of Se in lambs. Dietary Se supplementation significantly improved (P?<?0.001) glutathione peroxidase activity in blood. Furthermore, at the end of the trial, serum tri-iodothyronine (T3) amount also increased (P?<?0.05), while serum thyroxine (T4) amount decreased (P?<?0.05). Digestibility of dry matter, organic matter, crude protein, neutral detergent fiber, and acid detergent fiber increased (P?<?0.05) by Se yeast supplementation. It may be concluded that supplementation of Se in lambs had no significant effect on performance and blood hematology, but increased blood glutathione peroxidase activity and serum T3 amount and decreased serum T4 amount as compared to non-supplemented control lambs. Furthermore, Se yeast improved nutrient digestibility in lambs.     

Colostrum and milk selenium,antioxidative capacity and immune status of dairy cows fed sodium selenite or selenium yeast

Dietary selenium (Se) can be supplemented from organic or inorganic sources and this may affect Se metabolism and functional outcome such as antioxidative status and immune functions in dairy cows. A feeding trial was performed with 16 Holstein-Friesian dairy cows fed with a total mixed ration (0.18 mg Se/kg dry matter (DM)) either without Se supplement (Control, n = 5), or with Se from sodium selenite (Group SeS, n = 5) or Se yeast (Group SeY, n = 6). In Groups SeS and SeY, the Se supplementation amounted to an additional intake of 4 mg Se and 6 mg Se/d during gestation and lactation, respectively. The effect of both Se sources was characterised by milk Se and antioxidant levels, and the phenotyping and functional assessment of phagocytic activity of milk immune cells. Se yeast has been found to increase (p ≤ 0.001) the milk Se and antioxidant levels markedly compared to the control group. The experimental treatment did not affect the immune parameters of the cows. Lymphocyte subpopulations and phagocytosis activity of neutrophilic granulocytes were affected neither by the Se intake nor by the two different dietary supplements. It can be concluded that sodium selenite and Se yeast differ considerably in their effects on antioxidant status in dairy cows. However, the basal dietary Se concentration of 0.18 mg/kg DM seemed to be high enough for the measured immune variables.     

Nitric oxide exacerbates Al-induced inhibition of root elongation in rice bean by affecting cell wall and plasma membrane properties

Aluminum (Al) toxicity is one of the most widespread problems for crop production on acid soils, and nitric oxide (NO) is a key signaling molecule involved in the mediation of various biotic and abiotic stresses in plants. Here we found that exogenous application of the NO donor sodium nitroprusside (SNP) exacerbated the inhibition of Al-induced root growth in rice bean [Vigna umbellata (Thunb.) Ohwi & Ohashi ‘Jiangnan’, Fabaceae]. This was accompanied by an increased accumulation of Al in the root apex. However, Al treatments had no effect on endogenous NO concentrations in root apices. These results indicate that a change in NO concentration is not the cause of Al-induced root growth inhibition and the adverse effect of SNP on Al-induced root growth inhibition should result from increased Al accumulation. Al could significantly induce citrate efflux but SNP had no effects on citrate efflux either in the absence or presence of Al. On the other hand, SNP pretreatment significantly increased Al-induced malondialdehyde accumulation and Evans Blue staining, indicating an intensification of the disruption of plasma membrane integrity. Furthermore, SNP pretreatment also caused greater induction of pectin methylesterase activity by Al, which could be the cause of the increased Al accumulation. Taken together, it is concluded that NO exacerbates Al-induced root growth inhibition by affecting cell wall and plasma membrane properties.     

Evaluation of the protective activity of deferiprone, an aluminum chelator, on aluminum-induced developmental toxicity in mice

BACKGROUND: Since deferiprone can be an effective chelating agent for the treatment of aluminum (Al) overload, in the present study we investigated whether this chelator could protect against Al-induced maternal and developmental toxicity in mice. METHODS: A single oral dose of Al nitrate nonahydrate (1,327 mg/kg) was given on gestation day 12, the most sensitive time for Al-induced maternal and developmental toxic effects in mice. At 2, 24, 48, and 72 hr thereafter, deferiprone was given by gavage at 0 and 24 mg/kg. Cesarean sections were performed on day 18 of gestation and fetuses were examined for malformations and variations. RESULTS: Aluminum-induced maternal toxicity was evidenced by significant reductions in body weight gain, corrected body weight change, and food consumption. Developmental toxicity was evidenced by a significant decrease in fetal weight per litter and an increase in the total number of fetuses and litters showing bone retardation. No beneficial effects of deferiprone on these adverse effects could be observed. By contrast, a more pronounced decrease in maternal weight gain and corrected body weight change, as well as a higher number of litters with fetuses showing skeletal variations was noted in the group exposed to Al nitrate and treated with deferiprone at 24 mg/kg. CONCLUSIONS: According to the current results, deferiprone would not be effective to prevent Al-induced maternal and embryo/fetal toxicity in mice.     

The Effect of Selenium on the Cd-Induced Apoptosis via NO-Mediated Mitochondrial Apoptosis Pathway in Chicken Liver

Cd-induced apoptosis and the protective effects of Se against Cd-induced injury have been reported in previous studies. However, little is known regarding the effects of Cd-induced apoptosis in hepatic cells and the antagonistic effects of Se on Cd in poultry. In the present study, 128 healthy 31-week-old laying hens were randomly divided into four groups, which were fed basic diets, with the addition of Se (Na₂SeO₃, 2 mg/kg), Cd (CdCl₂, 150 mg/kg), or Se + Cd (150 mg/kg of CdCl₂ and 2 mg/kg of Na₂SeO₃) for 90 days. Ultrastructural changes, nitric oxide (NO) concentrations, inducible nitric oxide synthase (iNOS) activities, results of the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay of apoptosis, and the expression of iNOS and apoptosis-related genes in livers were determined. It was observed that Cd treatment significantly increased the concentrations of NO and iNOS activity in chicken livers. The production of excessive NO initiated the mitochondrial apoptotic pathway. Exposure to Cd increased the mRNA and the protein expression levels of iNOS, caspase-3, Bax, p53, and Cyt-c. Furthermore, the ratio of Bax/Bcl-2 increased, while the expression of Bcl-2 decreased. Treatment with Se significantly alleviated Cd-induced apoptosis in chicken livers, as evidenced by a reduction in the production of NO, iNOS activity, the number of apoptotic cells, and mRNA and protein expression levels of iNOS, caspase-3, Bax, and Cyt-c. It indicated that Cd induced NO-mediated apoptosis through the mitochondrial apoptotic pathway and Se exerted antagonizing effects. The present study provides new insights as to how Se affects Cd-induced toxicity in the chicken liver.     

Propofol Reduces Inflammatory Reaction and Ischemic Brain Damage in Cerebral Ischemia in Rats

Our previous studies demonstrated that inflammatory reaction and neuronal apoptosis are the most important pathological mechanisms in ischemia-induced brain damage. Propofol has been shown to attenuate ischemic brain damage via inhibiting neuronal apoptosis. The present study was performed to evaluate the effect of propofol on brain damage and inflammatory reaction in rats of focal cerebral ischemia. Sprague–Dawley rats underwent permanent middle cerebral artery occlusion, then received treatment with propofol (10 or 50 mg/kg) or vehicle after 2 h of ischemia. Neurological deficit scores, cerebral infarct size and morphological characteristic were measured 24 h after cerebral ischemia. The enzymatic activity of myeloperoxidase (MPO) was assessed 24 h after cerebral ischemia. Nuclear factor-kappa B (NF-κB) p65 expression in ischemic rat brain was detected by western blot. Cyclooxygenase-2 (COX-2) expression in ischemic rat brain was determined by immunohistochemistry. ELISA was performed to detect the serum concentration of tumor necrosis factor-α (TNF-α). Neurological deficit scores, cerebral infarct size and MPO activity were significantly reduced by propofol administration. Furthermore, expression of NF-κB, COX-2 and TNF-α were attenuated by propofol administration. Our results demonstrated that propofol (10 and 50 mg/kg) reduces inflammatory reaction and brain damage in focal cerebral ischemia in rats. Propofol exerts neuroprotection against ischemic brain damage, which might be associated with the attenuation of inflammatory reaction and the inhibition of inflammatory genes.     

Overexpression of MsALMT1, from the Aluminum-Sensitive Medicago sativa, Enhances Malate Exudation and Aluminum Resistance in Tobacco

Aluminum (Al) toxicity is a major limiting factor for plant growth and crop production in acidic soils. Al-induced organic acid (OA) exudation plays an important role in plant Al resistance. The exudation of OAs is mediated by membrane-localized OA transporters. In our previous study, a gene encoding the Al-induced malate transporter (MsALMT1) was identified in the roots of the Al-sensitive plant Medicago sativa L. cv. Yumu no. 1 (YM1). To further validate the function of MsALMT1, transgenic plants that overexpressed MsALMT1 under the control of the CaMV 35S (35S) promoter were generated. This transgenic tobacco showed an enhanced capacity for malate efflux and better Al resistance than wild type (WT) plants after exposure to 30 μM Al for 24 h. The Al content in the transgenic plant roots decreased to 40–52 % of that in WT plant roots. These results demonstrate that MsALMT1 is an Al-resistant gene in YM1 and encodes a malate transporter, the overexpression of which effectively enhances the Al resistance of transgenic tobacco plants.     

Effects of Zinc and <Emphasis Type="Italic">N</Emphasis>-Acetylcysteine in Damage Caused by Lead Exposure in Young Rats

This study investigated the toxicity of rats exposed to lead acetate (AcPb) during the second phase of brain development (8–12 days postnatal) in hematological and cerebral parameters. Moreover, the preventive effect of zinc chloride (ZnCl₂) and N-acetylcysteine (NAC) was investigated. Pups were injected subcutaneously with saline (0.9% NaCl solution), ZnCl₂ (27 mg/kg/day), NAC (5 mg/kg/day) or ZnCl₂ plus NAC for 5 days (3rd–7th postnatal days), and with saline (0.9% NaCl solution) or AcPb (7 mg/kg/day) in the five subsequent days (8th–12th postnatal days). Animals were sacrificed 21 days after the last AcPb exposure. Pups exposed to AcPb presented inhibition of blood porphobilinogen-synthase (PBG-synthase) activity without changes in hemoglobin content. ZnCl₂ pre-exposure partially prevented PBG-synthase inhibition. Regarding neurotoxicity biomarkers, animals exposed to AcPb presented a decrease in cerebrum acetylcholinesterase (AChE) activity and an increase in Pb accumulation in blood and cerebrum. These changes were prevented by pre-treatment with ZnCl₂, NAC, and ZnCl₂ plus NAC. AcPb exposure caused no alteration in behavioral tasks. In short, results show that AcPb inhibited the activity of two important enzymatic biomarkers up to 21 days after the end of the exposure. Moreover, ZnCl₂ and NAC prevented the alterations induced by AcPb.     

Neuroprotective effect of quercetin in ectoenzymes and acetylcholinesterase activities in cerebral cortex synaptosomes of cadmium-exposed rats

This study investigated the effect of quercetin on nucleoside triphosphate diphosphohydrolase (NTPDase), 5′-nucleotidase, adenosine deaminase (ADA), and acetylcholinesterase (AChE) activities in synaptosomes from cerebral cortex of adult rats exposed to cadmium (Cd). Rats were exposed to Cd (2.5 mg/Kg) and quercetin (5, 25 or 50 mg/Kg) by gavage for 45 days. Rats were randomly divided into eight groups (n = 8–10): saline/ethanol, saline/Querc 5 mg/kg, saline/Querc 25 mg/kg, saline/Querc 50 mg/kg, Cd/ethanol, Cd/Querc 5 mg/kg, Cd/Querc 25 mg/kg, and Cd/Querc 50 mg/kg. Results demonstrated that AChE activity increased in the Cd/ethanol group when compared to saline/ethanol group. Treatment with quercetin prevented the increase in AChE activity when compared to Cd/ethanol group. Quercetin treatment prevented the cadmium-induced increase in NTPDase, 5-nucleotidase, and ADA activities in Cd/ethanol group when compared to saline/ethanol group. Our data showed that quercetin have a protector effect against Cd intoxication. This way, is a promising candidate among the flavonoids to be investigated as a therapeutic agent to attenuate neurological disorders associated with Cd intoxication.     

Morphological changes in the apex of pea roots during and after recovery from aluminium treatment

We investigated how the pea (Pisum sativum cv. Harunoka) root, upon return to an Al-free condition, recovers from injury caused by exposure to Al. The growing region of the root during and after treatment with Al was examined by marking the root at intervals with India ink. Al-induced cell death was detected by staining with Evans blue. Root growth in 40 μM Al solution relative to that in Al-free solution (RRG) was approximately 45% from 6 h to12 h after the start of the treatment. However, values of RRG from 12 h to 24 h in Al-free solution for recovery or in the same Al solution were about 75% and 35%, respectively, indicating recovery from Al-induced growth inhibition. Images of the root characterized by zonal staining with Evans blue were observed in the sub-apical region (more than 1 mm from the tip) in Al-stressed roots. However, the interval of the stained zone was widened in the root after recovery from Al-induced growth inhibition, though it was narrower and more densely stained with time in the Al-stressed roots. During the recovery, the root apex may resume elongation in a specified region without Al-induced death or injury in cells detected by Evans blue.     

Serum Concentrations of 15 Elements Among <Emphasis Type="Italic">Helicobacter Pylori</Emphasis>-Infected Residents from Lujiang County with High Gastric Cancer Risk in Eastern China

Data on the effects of magnesium-zinc-calcium-vitamin D co-supplementation on hormonal profiles, biomarkers of inflammation, and oxidative stress among women with polycystic ovary syndrome (PCOS) are scarce. The objective of this study was to assess the effects of magnesium-zinc-calcium-vitamin D co-supplementation on hormonal profiles, biomarkers of inflammation, and oxidative stress in women with PCOS. Sixty PCOS women were randomized into two groups and treated with 100 mg magnesium, 4 mg zinc, 400 mg calcium plus 200 IU vitamin D supplements (n = 30), or placebo (n = 30) twice a day for 12 weeks. Hormonal profiles, biomarkers of inflammation, and oxidative stress were assessed at baseline and at end-of-treatment. After the 12-week intervention, compared with the placebo, magnesium-zinc-calcium-vitamin D co-supplementation resulted in significant reductions in hirsutism (?2.4 ± 1.2 vs. ?0.1 ± 0.4, P < 0.001), serum high sensitivity C-reactive protein (?0.7 ± 0.8 vs. +0.2 ± 1.8 mg/L, P < 0.001), and plasma malondialdehyde (?0.4 ± 0.3 vs. +0.2 ± 1.0 μmol/L, P = 0.01), and a significant increase in plasma total antioxidant capacity concentrations (+46.6 ± 66.5 vs. ?7.7 ± 130.1 mmol/L, P = 0.04). We failed to find any significant effect of magnesium-zinc-calcium-vitamin D co-supplementation on free androgen index, and other biomarkers of inflammation and oxidative stress. Overall, magnesium-zinc-calcium-vitamin D co-supplementation for 12 weeks among PCOS women had beneficial effects on hormonal profiles, biomarkers of inflammation, and oxidative stress.