(-)-α-bisabolol exerts neuroprotective effects against pentylenetetrazole-induced seizures in rats by targeting inflammation and oxidative stress.

Epilepsy is the most common neurological disorder which is accompanied with behavioral and psychiatric alternations. Current evidences have shown that (-)-α-bisabolol (BSB) possess anti-inflammatory and antioxidative effects in several animal studies. Here, we conducted present study to evaluate its neuroprotective effects against pentylenetetrazole (PTZ)-induced seizures in rats. We used fifty male rats and they were randomly assigned into 5 groups control, BSB100, PTZ, BSB50 + PTZ, BSB100 + PTZ. The animals intraperitoneally received PTZ (45 mg/kg) for ten consecutive days to induce epilepsy model. BSB in doses of 50 and 100 mg/kg was administrated orally one hour before PTZ administration for ten days. The elevated plus maze (EPM) test was carried out to assess anxiety-like behavior. The seizure intensity was evaluated according to modifies Racine's convulsion scale (RCS). Y-maze and passive avoidance were utilized to assess working memory and aversive memory. The expression of pro-inflammatory cytokines and oxidative stress factors were measured using the enzyme-linked immunosorbent assay (ELISA). The neuronal cell loss in the hilar region was assessed using Nissl staining. Results showed that PTZ-treated rats had more seizure intensity, anxiety-like behavior, memory deficits, higher levels of TNF-α, IL-1ß, and oxidative markers. Pre-treatment with BSB 100 significantly inhibited seizure intensity, anxiety-like behavior, and memory deficits; reduced levels of TNF-α, IL-1ß, and MDA oxidative markers. Collectively, outcome of this work shows that BSB at the dose of 100 mg/kg may exert neuroprotective effects by mitigating seizures, oxidative stress, and neuroinflammation, and ameliorates memory and anxiety disorders in the PTZ-induced seizure rats.

Alpha-pinene moderates memory impairment induced by kainic acid via improving the BDNF/TrkB/CREB signaling pathway in rat hippocampus.

Introduction: The potential benefits of natural ingredients in the alleviation of neurodegenerative disorders are of great interest. Alpha-pinene (APN) is an essential oil belonging to monoterpenes with multiple beneficial effects. In this study, the possible improving effects of alpha-pinene on memory impairment induced by kainic acid and the underlying molecular mechanisms were examined. Methods: Memory impairment was induced by i.c.v. injection of kainic acid (KA) in male Wistar rats. Alpha-pinene (50 mg/kg/day, i.p.) was injected for 21 days, including 14 days before the KA injection and seven days afterward. Spatial working memory and inhibitory avoidance (IA) memory performance were assessed five and even days following KA injection, respectively. The hippocampal protein levels of brain-derived neurotrophic factor (BDNF), tropomyosin-like receptor kinase B (TrkB), cAMP response element binding protein (CREB), and neuronal loss in the CA1 region were also examined. Results: Results revealed that the i.c.v. injection of KA triggered memory impairment, which was notably diminished by alpha-pinene pre-and post-treatment. Histopathological evaluation revealed that alpha-pinene significantly moderated the attenuation in CA1 alive neurons induced by KA injection. Western blotting analysis confirmed that alpha-pinene pre-and post-treatment significantly reversed the KA-induced decreases in the hippocampal levels of BDNF, TrkB, phosphorylated TrkB, CREB, and phosphorylated CREB. Discussion: These findings suggest that alpha-pinene pre-and post-treatment moderate memory impairment induced by KA by restoring the BDNF/TrkB/CREB signaling pathway in the rat hippocampus.

Neuroprotective effects of Royal Jelly (RJ) against pentylenetetrazole (PTZ)-induced seizures in rats by targeting inflammation and oxidative stress.

Epilepsy is a chronic neurological condition in which inflammation and oxidative stress play a key role in the pathogenesis. Recently, several studies have suggested that Royal Jelly (RJ) has antioxidant effects. Nevertheless, there is no evidence of its effectiveness against epilepsy. Here, we evaluated its neuroprotective effects at different doses (100 and 200 mg/kg) against pentylenetetrazole (PTZ)-induced seizures. Fifty male Wistar rats were randomly divided into five groups: control, PTZ, RJ100 + PTZ, RJ200 + PTZ and RJ100. In order to establish epilepsy model, 45 mg/kg of PTZ was injected intraperitoneally for 10 consecutive days. Seizure parameters were graded based on Racine's 7-point classification. Elevated-plus maze, Y maze and shuttle box tests were carried out to assess anxiety-like behavior, short-term memory, and passive avoidance memory, respectively. We used ELISA technique to measure the expression of the pro-inflammatory cytokines and oxidative stress factors. Also, neuronal loss in the hippocampal CA3 region was determined using Nissl staining. Our findings showed that PTZ-treated rats had more seizure intensity, anxiety-like behavior, memory dysfunction, higher levels of TNF-α, IL-1ß, and oxidative markers. RJ could allay seizure severity and duration. It also improved memory function as well as anxiety level. In terms of biochemical assessment, RJ gave rise to a significant decrease in the level of IL-1ß, TNF-α and MDA and it restored the activities of GPX and SOD enzymes. Hence, our study shows that RJ contains anti-inflammatory and antioxidative effects which contribute to less neuronal damage in the PTZ-induced epilepsy model.

Anticonvulsant Effects of Royal Jelly in Kainic Acid-Induced Animal Model of Temporal Lobe Epilepsy Through Antioxidant Activity.

Temporal lobe epilepsy (TLE) is the most common form of partial and drug-resistant epilepsy, characterized by recurrent seizures originating from temporal lobe structures like the hippocampus. Hippocampal sclerosis and oxidative stress are two important factors in the pathogenesis of TLE that exacerbate epileptic seizures in this form of epilepsy. Recently, royal jelly (RJ) shown to have neuroprotective and antioxidant activities in several neurodegenerative models. Therefore, the aim of the present study was to investigate the pretreatment effect of RJ on epileptic seizures, hippocampal neuronal loss, and oxidative stress in the rat model of kainic acid (KA)-induced TLE. To this aim, 40 male Wistar rats weighing 200-250 g were divided into 4 groups, including control, vehicle, KA, and RJ + KA. Rats received RJ (150 mg/kg/day) for 14 days before induction of TLE with KA. Epileptic behaviors were evaluated according to Racine's scale. Oxidative stress markers including, malondialdehyde (MDA), total oxidant status (TOS) and total antioxidant capacity (TAC) as well as neuronal loss in the CA1 region of the hippocampus (using Nissl staining) were evaluated in all groups. Our findings showed that RJ pretreatment significantly reduced the seizure score and increased the latency to the first seizure. RJ also reduced MDA and TOS while increasing TAC. In addition, RJ reversed neuronal damage in the hippocampal CA1 and CA3 areas. In conclusion, our results suggest that RJ has anticonvulsant and neuroprotective effects in KA induced TLE via its antioxidative properties.

Alpha-Pinene Exerts Antiseizure Effects by Preventing Oxidative Stress and Apoptosis in the Hippocampus in a Rat Model of Temporal Lobe Epilepsy Induced by Kainate.

Oxidative stress and apoptosis following seizures play pivotal roles in the consequences of repeated seizures. Beneficial effects of alpha-pinene (APN) have been reported in some experimental models of neurodegenerative diseases. However, its neuroprotective efficacy in a rat model of temporal lobe epilepsy (TLE) induced by kainic acid (KA) has remained unexplored. We aimed to explore the possible antiseizure effects of APN pretreatment and underlying molecular mechanisms in a rat model of TLE induced by KA. TLE was induced in male Wistar rats by intracerebroventricular injection of KA. APN at a dose of 50 mg/kg/day was intraperitoneally injected for 2 weeks before induction of TLE. One day after the induction of TLE, behavioral expressions of seizure were recorded and scored using Racine's scale. Furthermore, the hippocampal levels of oxidative stress markers, B-cell lymphoma 2 (Bcl2), BCL2-associated X protein (BAX), and c-Jun N-terminal kinase (JNK) protein levels were also assessed. Histopathological assessment in the hippocampus was performed with Nissl staining 5 days following induction of TLE. The results revealed that APN pretreatment alleviated epileptic seizures, diminished oxidative stress indicators, blocked the mitochondrial apoptotic pathway via decreasing BAX and raising BCL2 protein levels in the hippocampus at least partly through inhibiting JNK activity, and decreased neuronal death in the CA3 and hilus regions. These findings reveal that APN pretreatment mitigates KA-induced seizures by blocking oxidative stress and neuronal damage factors. It can be concluded that APN has a potent potential to be considered an antiseizure medication, but it needs further investigation.

Alpha-Pinene Alleviates Motor Activity in Animal Model of Huntington's Disease via Enhancing Antioxidant Capacity.

Huntington's disease (HD) is a progressive, neurodegenerative, and inherited disease. Antioxidants have been shown to be effective in slowing disease progression in animal models of HD and are under investigation in human clinical trials. α-pinene, a member of the monoterpene class, has been shown to exert antioxidant activity. Therefore, this study aimed to investigate the impact of α-pinene on animal model of HD. Thirty-two male Wistar rats received 3-Nitropropionic acid (3-NP) for induction of the disease model or treated with α-pinene + 3-NP in different groups. Motor skill, and biochemical evaluations to detect oxidant/antioxidant markers in rat cortex and striatum were performed in all groups. We found that α-pinene significantly improved 3-NP-induced changes in the body weight, rotarod activity, time taken to cross the narrow beam, and locomotor activity. Biochemical analysis revealed that α-pinene significantly decreased the 3NP-induced elevation in oxidant markers, nitrite, and malondialdehyde in both cortex and striatum. In addition, α-pinene counteracted the 3-NP-induced fall in antioxidant enzymes, including superoxide dismutase, catalase, and glutathione in the cortex and striatum. In conclusion, we found that α-pinene prevented the motor dysfunction induced by 3-NP in the animal model of Huntington's disease. Oxidants-antioxidant balance might be involved in the protective effect of α-pinene.

Investigating the mechanism of antiepileptogenic effect of apigenin in kainate temporal lobe epilepsy: possible role of mTOR.

Clarifying the underlying mechanisms of epileptogenesis is important in preventing the progression of chronic epilepsy. In epilepsy, the mTOR (mammalian target of rapamycin) pathway plays a critical role in mediating the mechanism of epileptogenesis. In this study, we investigate whether apigenin can exert antiepileptogenic effects through the inhibition of mTOR in the kainate model of epilepsy. For assessing the antiepileptogenic effect of apigenin in kainic acid (KA)-induced temporal lobe epilepsy (TLE) model, apigenin at a dose of 50 mg/kg was administrated by gavage for 6 days. An intracranial electroencephalogram (iEEG) was performed to confirm the establishment of status epilepticus. BrdU was used to detect neurogenesis in the CA3, and dentate gyrus and mossy fiber sproutings were assessed by Timm staining. The expression of mTOR was quantified via western blot. We found that apigenin-pretreatment had a significant inhibitory effect on neural cell death, spontaneous seizure spikes, aberrant neurogenesis, mTOR hyperactivity, and aberrant mossy fiber sprouting. Overall, these results suggest that apigenin has an antiepileptogenic effect and may be a useful target for inhibiting mTOR hyperactivity in epilepsy.

Acetyl-L-Carnitine Exerts Neuroprotective and Anticonvulsant Effect in Kainate Murine Model of Temporal Lobe Epilepsy.

The most well-known type of focal epilepsy that is resistant to existing treatments is temporal lobe epilepsy (TLE), with seizure foci in various structures including temporal lobe, hippocampus, amygdala, entorhinal cortex, and subcortex. The most significant processes involved in the pathophysiology of temporal lobe epilepsy (TLE) are oxidative stress, inflammation, and pyroptosis. There are evidences indicating that acetyl-l-carnitine (ALC) has anti-oxidative, anti-inflammatory, and anti-pyroptotic effects. In the present study, rat model of TLE was induced by intrahippocampal kainate and animals received ALC (100 mg/kg, p.o.). ALC properly attenuated intensity of seizures and also incidence of kainate-induced status epilepticus (SE). As well, obtained findings showed that ALC can partially reverse hippocampal levels of MDA, ROS, SOD, TNFa, NF-kB, TLR4, GFAP, and caspase 1. Besides, treatment of kainate group with ALC exerted a protective effect against CA1 neuronal loss and abnormal mossy fiber sprouting (MFS). Conclusively, these results suggest that ALC is capable to attenuate kainate-induced SE which is somewhat mediated through its lowering of oxidative stress, neuroinflammation, and pyroptosis that are related to its neuroprotective effect.

Prevalence of depression, anxiety, and psychological distress in patients with epilepsy during COVID-19: A systematic review.

OBJECTIVE: COVID-19 pandemic disease has profound consequences for physical and mental health. In this regard, health care for chronic diseases, especially epilepsy is neglected The purpose of this systematic review study was to investigate the epidemic effect of COVID-19 on increasing the prevalence of mental disorders such as depression, anxiety, and sleep disorders in people with epilepsy (PWE). METHODS: We systematically searched MEDLINE, Cochrane, Embase, Web of science, Scopus, and Psych info databases for studies that estimate the prevalence of mental disorders in PWE during the COVID-19 until December 2020. Inclusion criteria included samples of population, with a confirmed diagnosis of epilepsy. RESULTS: Irrespective of PWE or people without epilepsy (PWOE), all experienced stress and anxiety during COVID-19 pandemic. Most of the studies showed that PWE and even PWOE during the pandemic, suffer from depression. The highest rate of depression was attributed to female PWE with financial problems (66.7%) and the lowest rate of depression in PWE was reported in 8.6%. 7.1-71.2% and 28.2% of patients reported sleep disorders and insomnia, respectively. Less than 2% experienced a sleep improvement. LIMITATIONS: Due to a large amount of heterogeneities across the results, we could not evaluate the exact rate of prevalence in spite of using effective measures. CONCLUSIONS: People with epilepsy were considered as a susceptible group to the impact of the pandemic. Therefore, great attention should be paid to PWE and adequate psychological supports provided in this period to relieve or inhibit risks to mental health in PWE.

Evaluation of the ameliorative effects of oral administration of metformin on epileptogenesis in the temporal lobe epilepsy model in rats.

AIMS: Understanding the underlying molecular mechanisms involved in epileptogenesis is necessary to target the best therapeutic interventions in epilepsy. Recently, it has been postulated that metformin, an old antidiabetic oral drug, has anti-seizure properties mostly due to its antioxidant activities. This study was designed to evaluate the ameliorative effects of metformin on the progression of epilepsy in the temporal lobe epilepsy model in rats. MAIN METHODS: Temporal lobe Epilepsy was induced by intracerebroventricular microinjection of kainic acid. Metformin was orally administered for two weeks before induction of epilepsy. Anti-epileptogenic activity of metformin was evaluated by intracranial electroencepholography (IEEG) recording to detect spontaneous seizures, mossy fiber sprouting by Timm staining, neurogenesis by BrdU staining. KEY FINDINGS: Oral administration of metformin prior to kainite-induced status epilepticus blocked the variant characterizations of epileptogenesis like neuronal cell death, aberrant neurogenesis, mossy fiber sprouting, and spontaneous seizures. SIGNIFICANCE: These findings indicate that metformin has potential anti-epileptogenic properties in temporal lobe epilepsy.

Effects of Hair Follicle Stem Cells on Partial-Thickness Burn Wound Healing and Tensile Strength

Background: The recent improvements in wound healing have led to new strategies in regenerative medicine. Burn wound healing is an important issue in skin regeneration and has multiple indications for stem cell therapy. Hair follicle stem cells (HFSCs) are a highly promising source of stem cells for healing use, as these cells are accessible, active and pluripotent adult stem cells. Methods: HFSCs of the rat whisker were isolated, cultured, and labeled with DiI. Flow cytometry method was used to detect special markers of HFSCs. Deep partial-thickness burn wound was created, and labeled HFSCs were injected around the wound bed. Wound closure was recorded via digital photographs. The inflicted rats were sacrificed at 3, 7, or 14 days post burn and used for subsequent histological and tensiometry analysis. Results: Our results indicated that HFSCs were positive for Nestin and CD34 markers, but negative for Kr15. Morphological and histological photographs revealed that wound closure rate was accelerated in stem cell-treated group compared with other groups. In addition, faster re-epithelialization and collagen deposition were observed. The immunohistochemical analysis suggested that CD31 expression and vascular density enhanced in the stem cell-treated group. Further, tissue tensile strength increased in HFSCs-treated rats in comparison to the control group. Conclusion: The present study demonstrates that HFSC could accelerate burn wound healing as well as tensile strength in rats.

In vitro Differentiation of Hair Follicle Stem Cell into Keratinocyte by Simvastatin

Background: Hair follicle stem cells (HFSCs) located in the bulge area has shown to be highly proliferative and could differentiate into neurons, glia, smooth muscle cell, and melanocytes in vitro. Simvastatin is an HMG-CoA reductase inhibitor that exerts pleiotropic effects beyond simple low-density lipoprotein lowering and has a similar impact on the differentiation of bone marrow stromal cells and peripheral blood mononuclear cells. The present study examined the hypothesis that the application of simvastatin would induce the HFSCs differentiation into keratinocyte. Methods: The bulge of the hair follicle was anatomized, and HFSCs were cultivated. The flow cytometry and immunocytochemical staining for detection of nestin, CD34, and Kr15 biomarkers were performed before differentiation. In order to hasten the HFSCs differentiation to keratinocyte, HFSCs were treated with 1 µM, 2 µM, and 5 µM of simvastatin daily for a week. After differentiation, the flow cytometry and immunocytochemical staining were performed with Kr15 and Kr10 biomarkers, and the MTT assay was carried out as an index of cell viability and cell growth. Results: Our results showed that bulge of HFSCs were nestin and CD34 positive and Kr15 negative. Simvastatin significantly increased the viability of HFSCs (p < 0.05) at the concentration of 5 µM. In addition, the percentages of keratinocyte-differentiated cells treated with 5 µM of simvastatin showed a significant increase compared to all other treated groups (p < 0.05). Conclusion: Our findings demonstrate that 5 µM of simvastatin could induce HFSCs differentiation into keratinocyte.

Evaluation of the neuroprotective, anticonvulsant, and cognition-improvement effects of apigenin in temporal lobe epilepsy: Involvement of the mitochondrial apoptotic pathway.

OBJECTIVES: Cognitive deficit is a common problem in epilepsy. A major concern emergent from the use of antiepileptic drugs includes their side effects on learning and memory. Herbal medicine is considered a complementary and alternative therapy in epilepsy. Apigenin is a safe flavone with antioxidant properties. However, there is little information about the beneficial effect of apigenin on cognition in epilepsy. MATERIALS AND METHODS: For evaluating the anticonvulsant effect of apigenin in the kainite temporal epilepsy model, apigenin was orally administered at 50 mg/kg for six days. Reference and working memory were examined via the Morris water maze and Y-maze task spontaneously. RESULTS: Results showed that apigenin had significant anticonvulsant activity (P<0.01) and restored the memory-deficit induced by kainic acid (P<0.05). Furthermore, apigenin significantly increased the number of living neurons in the hilus (P<0.001). Immunohistochemical analysis showed that apigenin reduced the release of cytochrome c (P<0.01), suggesting an inhibitory role in the intrinsic apoptotic pathway. CONCLUSION: These results suggest that apigenin restores memory impairment via anticonvulsant and neuroprotective activity.

Interactive effects of prenatal exposure to restraint stress and alcohol on pentylenetetrazol-induced seizure behaviors in rat offspring.

Prenatal exposure to stress or alcohol increases vulnerability of brain regions involved in neurobehavioral development and programs susceptibility to seizure. To examine how prenatal alcohol interferes with stress-sensitive seizures, corticosterone (COS) blood levels and pentylenetetrazol (PTZ)-induced seizure behaviors were investigated in rat pups, prenatally exposed to stress, alcohol, or both. Pregnant rats were exposed to stress and saline/alcohol on 17, 18, and 19 days of pregnancy and divided into four groups of control-saline (CS), control-alcohol (CA), restraint stress-saline (RS), and restraint stress-alcohol (RA). In CS/CA groups, rats received saline/alcohol (20%, 2 g/kg, intraperitoneally [i.p.]). In RS/RA groups, rats were exposed to restraint stress by being held immobile in a Plexiglas® tube (twice/day, 1 h/session), and received saline/alcohol, simultaneously. After parturition, on postnatal days 6 and 15 (P6 & P15), blood samples were collected from the pups to determine COS level. On P15 and P25, PTZ (45 mg/kg) was injected into the rest of the pups and seizure behaviors were then recorded. COS levels increased in pups of the RS group but not in pups of the RA group. Both focal and tonic-clonic seizures were prevalent and severe in pups of the RS group, whereas only focal seizures were prominent in pups of the CA group. However, pups prenatally exposed to co-administration of alcohol and stress, unexpectedly, did not show additive epileptic effects. The failure of pups prenatally exposed to alcohol to show progressive or facilitatory epileptic responses to stressors, indicates decreased plasticity and adaptability, which may negatively affect HPA-axis performance or hippocampal structure/function.

Interaction of prenatal stress and morphine alters prolactin and seizure in rat pups.

Prenatal exposure to stress and morphine has complicated effects on epileptic seizure. In the present study, effect of prenatal forced-swim stress and morphine co-administration on pentylenetetrazol (PTZ) induced epileptic behaviors and prolactin blood level (PBL) was investigated in rat offspring. Pregnant Wistar rats were divided to four groups of control-saline, control-morphine, stressed-saline and stressed-morphine. In the stressed group, pregnant rats were placed in 25°C water on gestation days 17, 18 and 19 (GD17, GD18 and GD19) for 30 min. In the morphine/saline group, pregnant rats received morphine (10, 12 and 15 mg/kg, IP, on GD17, GD18 and GD19, respectively) or saline (1 ml, IP). In the morphine/saline-stressed group, the rats received morphine or saline and then exposed to stress. On postnatal days 6 and 15 (P6 and P15), blood samples were obtained and PBL was determined. At P15 and P25, the rest of the pups was injected with PTZ to induce seizure. Then, epileptic behaviors of each rat were observed individually. Latency of first convulsion decreased in control-morphine and stressed-saline groups while increased in stressed-morphine rats compared to control-saline group on P15 (P=0.04). Number of tonic-clonic seizures significantly increased in control-morphine and stressed-saline rats compared to control-saline group at P15 (P=0.02). PBL increased in stressed-saline, control-morphine and stress-morphine groups compared to control-saline rats. It can be concluded that prenatal exposure of rats to forced-swim stress and morphine changed their susceptibility to PTZ-induced seizure and PBL during infancy and prepubertal period. Co-administration of morphine attenuated effect of stress on epileptic behaviors.

Effect of prenatal forced-swim stress and morphine co-administration on pentylentetrazol-induced epileptic behaviors in infant and prepubertal rats.

Prenatal exposure to stress and morphine has complicated effects on epileptic seizure. Many reports have shown an interaction between morphine- and stress-induced behavioral changes in adult rats. In the present study, effect of prenatal forced-swim stress and morphine co-administration on pentylentetrazole (PTZ)-induced epileptic behaviors was investigated in rat offspring to address effect of the interaction between morphine and stress. Pregnant rats were divided to four groups of control-saline, control-morphine, stressed-saline and stressed-morphine. In the stressed group, the rats were placed in 25 °C water on 17-19 days of pregnancy. In the morphine/saline group, the rats received morphine/saline on the same days. In the morphine/saline-stressed group, they were exposed to stress and received morphine/saline simultaneously. On postnatal day 15 (P15), blood samples were collected to determine corticosterone (COS) level. On P15 and P25, PTZ was injected to the rest of pups to induce seizure. Then, epileptic behaviors of each rat were individually observed. Latency of tonic-colonic seizures decreased in control-morphine and stressed-saline groups while increasing in stressed-morphine rats compared to control-saline group on P15. Duration of tonic-colonic seizures significantly increased in control-morphine and stressed-saline rats compared to stressed-morphine and control-saline rats on P15, but not P25. COS levels increased in stressed-saline group but decreased in control-morphine group compared to control-saline rats. Body weight was significantly higher in morphine groups than saline treated rats. Prenatal exposure to forced-swim stress potentiated PTZ-induced seizure in the offspring rats. Co-administration of morphine attenuated effect of stress on body weight, COS levels, and epileptic behaviors.

Headspace solid-phase microextraction-gas chromatography method for the determination of valproic acid in human serum, and formulations using hollow-fiber coated wire.

A method was developed for the extraction of valproic acid (VPA) by hollow-fiber coated wire as a lab-made solid-phase microextraction (SPME) fiber and its determination by capillary gas chromatography in human serum and pharmaceutical formulations. In this study, a piece of copper wire coated by polypropylene hollow-fiber membrane was used as a SPME fiber, and its efficiency for the extraction of VPA from the headspace of samples prior to gas chromatographic analysis was evaluated. The optimum conditions of microextraction process were selected, and the limit of detection for VPA was found to be 85 microg L(-1) in solution and 1.7 mg L(-1) in human serum. A low detection limit, a wide linear dynamic range (0.25-100 mg L(-1)), good repeatability (RSD%<4 in formulations and RSD%<7 in serum samples) and a higher mechanical durability due to its metallic base are some of the most important advantages of the proposed fiber.