Protective Effect Of Selenium Research Articles

Involvement of TRP channels on fibromyalgiainduced pain

Fibromyalgia (FM) is a common chronic pain syndrome affecting up to 2% of the adult population.Several factors such as excessive oxidative stress and overload calcium ion (Ca2+) influx play main roles in the etiology of FM. Several pharmaceutical drugs such as antidepressants and voltage-gated calcium channel blockers are recommended for the treatment of FM; however, they fail to produce a satisfactory response in patients with FM because of the unclear etiology of the disease. Transient receptor potential (TRP) channels have six subfamilies and 27 members in human. Most of these channels are responsible in dorsal root ganglia (DRG) neurons for the Ca2+ permeation especially in neuronal cells. Expression level of the TRPM2 and TRPV1 channels are high in the DRG neurons and they show oxidative stress dependent activation (Tan and McNaughton 2016; Santos et al. 2018). The TRPM2 and TRPV1 channel expression levels in the DRG increased in different types of pain. Selenium as an antioxidant trace element is implicated as a neuroprotective agent in peripheral pain through the inhibition of apoptosis and regulation of the TRPM2 and TRPV1 channels (Kahya et al. 2017). Since a decade, a recent theory have argued that both supporting of intracellular antioxidant system and extracellular antioxidant administration may helpful in fibromyalgia for the inhibition of TRP channels mediated Ca2+ influx (Yüksel et al. 2017). In the oral presentation, I discussed novel effects of selenium on the treatment of irregular oxidative status and fibromyalgia by the regulation of TRPM2 and TRPV1 channels in rats. In conclusion, present literature information indicated that protective effects of selenium on TRPM2 and TRPV1 channels may novel approach to treat FM induced pain and mitochondrial oxidative stress. However, the subject should be clarified by further studies.

Mercury and selenium in the grass goby Zosterisessor ophiocephalus (Pisces: Gobiidae) from a mercury contaminated Mediterranean lagoon

Mercury (Hg) and its bioaccumulation are important in evaluating the health risk through fish consumption. In the Marano and Grado Lagoon a historical contamination originating from both mining and industrial sources is present.In this study the Hg levels in the grass goby and the protective effect of selenium (Se) were determined as a function of size, sex, sampling sites and season.Mercury often exceeded the limit for commercialisation, whereas Se was mostly constant being homeostatically regulated.The mean Se/Hg molar ratio showed about 40% of data >1.0 and the HBVSe index was on average equal to 0.0. Thus, grass goby of this area is not a Se source food indicated for pregnant and/or breastfeeding women, but its occasional consumption would appear to have no contraindications if integrated with other Se rich foods: the ingestion of about 10 fish fillets per week can be safely consumed by adults.

Radiation Protective Effect of Selenium and Folic Acid Mixtures in the Development of Congenital Anomalies Following Radiation Exposure to the Fetus of Perinatal Female W hite R ats

Radiation Protective Effect of Selenium and Folic Acid Mixtures in the Development of Congenital Anomalies Following Radiation Exposure to the Fetus of Perinatal Female W hite R ats

Protective Effects of Selenium on Cyclophosphamide-Induced Oxidative Stress and Kidney Injury.

Cyclophosphamide (CP) is a common anticancer drug, but its use in cancer treatment is limited due to its severe toxicities induced mainly by oxidative stress in normal cells. Reactive oxygen species (ROS) lead to multiple organ injuries, including the kidneys. Selenium (Se) is a nutritionally essential trace element with antioxidant properties. In the present study, the possible protective effect of Se on CP-induced acute nephrotoxicity was investigated. Forty-two Sprague-Dawley rats were equally divided into six groups of seven rats in each. The control group received saline, and other groups were injected with CP (150mg/kg), Se (0.5 or 1mg/kg), or CP + Se intraperitoneally. Total antioxidant capacity (TAC), total oxidant state (TOS), oxidative stress index (OSI), creatinine, and cystatin C (Cys C) levels were measured in the sera. In addition, kidney tissues were examined histologically. In the CP alone treated rats, creatinine, Cys C, TOS, and OSI levels increased, while TAC level decreased. CP-induced histological damages were decreased by co-treatment of Se and biochemical results supported the microscopic observations. In conclusion, our study points to the therapeutic potential of Se and indicates a significant role of ROS in CP-induced kidney toxicity.

The Protective Effect of Selenium on Bovine Mammary Epithelial Cell Injury Caused by Depression of Thioredoxin Reductase.

To elucidate the effect of selenium (Se) on antioxidant function of mammary glands in dairy cows and the underlying mechanism, an experiment was conducted using a single-factor completely randomized design study. Bovine mammary epithelial cells (BMECs) were randomly divided into four groups: control, Se treatment, 2,4-dinitrochlorobenzene (DNCB) inhibition, and Se prevention. Treatment of BMECs with Se was found to significantly reverse decreased cell proliferation and the expression of thioredoxin reductase (TrxR) after DNCB exposure. DNCB-induced activation of apoptosis signaling kinase-1 (ASK-1), which activates the mitogen-activated protein kinase (MAPK) pathway, was reduced in BMECs treated with Se. Additionally, our results indicated that Se treatment resulted in lower intracellular accumulation of arachidonic acid (ARA) and 15-hydroperoxyeicosatetraenoic acid (15-HPETE) due to suppressed expression of cytosolic phospholipase A2 (cPLA2) regulated by p38MAPK and c-Jun N-terminal kinase (JNK) in DNCB-stimulated BMECs. Taken together, these findings suggest that Se treatment improved the antioxidant function of dairy cow mammary glands and protected cells from oxidative damage primarily by increasing the activity of TrxR, inhibiting the activation of the MAPK signaling pathway, and thus decreasing the content of ARA and its related metabolites.

The Protective Effect of Selenium on the Chicken Pancreas against Cadmium Toxicity via Alleviating Oxidative Stress and Autophagy.

Cadmium (Cd) is a highly toxic heavy metal that can affect human and animal health. Selenium (Se) is an essential microelement that can protect various organs against toxic heavy metals. Although many studies have investigated the adverse effect of Cd in rats and several other animals, little is known regarding the mechanisms of Cd-induced autophagy in the chicken pancreas and the antagonistic effect of Se on Cd. In the current study, we fed chickens Se, Cd, or Se and Cd supplements to establish the Se and Cd interaction model and to measure the concentrations of Se and Cd in the chicken pancreas. The ultrastructure changes of the chicken pancreas were also observed, and we detected oxidative stress indexes in each group. The expression levels of autophagy-related genes were also examined. We found that Cd exposure could increase the concentration of Cd, the activities of total superoxide dismutase (T-SOD), catalase (CAT), and glutathione peroxidase (GSH-Px); and the total antioxidant capacity (T-AOC) content in the chicken pancreas. The protein expression levels of dynein, Beclin1, LC3-1, LC3-2, and Atg5 were increased and that of TOR was decreased under Cd exposure conditions. However, the changes induced by Cd were significantly alleviated by Se. This study suggested that Cd could accumulate in the chicken pancreas and lead to oxidative stress and autophagy. Se was shown to antagonize Cd toxicity though reducing Cd accumulation, alleviating oxidative stress, and inhibiting autophagy. This study revealed a concrete mechanism for the Se antagonism of Cd and might provide a new clue for the detoxification of Cd poisoning.

The ameliorating effects of selenium and vitamin C against fenitrothion-induced blood toxicity in Wistar rats

Fenitrothion is widely used organophosphate pesticide in agriculture and health programs, but besides, it causes several toxic effects. The present study was designed to evaluate the possible protective effects of selenium (0.5mg/kg b.w.) and vitamin C (100mg/kg b.w) on altered haematological, biochemical and oxidative stress parameters in the blood of rats orally treated with fenitrothion (20mg/kg b.w) for 30days. Fenitrothion caused changes in body weight, food and water intake, and some haematological and biochemical parameters. Fenitrothion altered the glutathione redox status (GSH and GSSG) and decreased activity of antioxidant enzymes (GSH-Px, GST, SOD and CAT), leading to a lipid peroxidation. Selenium and vitamin C, by improving the activity of antioxidants, reduced oxidative stress and a lipid peroxidation, maintaining the values of examined parameters to optimal levels. Therefore, selenium and vitamin C could be useful in providing protection of exposed non-target organisms including people from fenitrothion.

Protective effect of selenium against aluminium chloride induced cardiotoxicity in rats

Protective effect of selenium against aluminium chloride induced cardiotoxicity in rats

Protecting Role of Selenium on the Cytotoxic Effect of Profenofos on Rabbit Fertility

Profenofos is an Organophosphorous compound and acaricide used in Egypt with cumulative toxic effects causing reproductive dysfunction and increase in reactive oxygen species production. Protective and anti-oxidant effects of selenium can improve the activity of radical scavenger. So, the aim of this study was to elucidate the protective effects of Selenium against reproductive toxicity induced by Profenofos in male and female New Zealand rabbits (n=18). Three experimental groups (3 males and 3 females per each group) receiving a combination of Profenofos (70 mg/ kg b. w.) and/or selenium in drinking water (25 mg/ kg b. w.) for 90-day was divided as follows: non treated (control), Profenofos alone and Profenofos + selenium group. Profenofos caused a decrease in body and organs weights compared to control group. It had a fetotoxic effect resulting in a significant reduction in pregnancy rate and the number of viable feti in treated animals. Also, Profenofos caused a significant elevation in ALT, AST, MDA, urea and creatinine, while a significant decrease was noticed in SOD, GSH, testosterone, estrogen and progesterone in all treated rabbits compared to control group. Concomitant administration of selenium with Profenofos alleviated the induced alterations. In addition to, histopathological results revealed that testes, epididymis, ovary and uterus alterations represented by degenerative and inflammatory changes as a result of Profenofos exposure. Profenofos had a carcinogenic effect on uterus as leiomyoma with rhabdomyosarcoma which gave positive immunoreactivity with Desmin and Smooth muscle actin. Also, Profenofos caused histopathological and histochemical effects in liver and kidney tissues. There was intensive positive immunoreactivity for caspase- 3 (dark brown granules) was observed in the cytoplasm of apoptotic testicular, ovarian and uterine cells that indicating the severity of Profenofos toxicity. On the other hand, examined tissues of Profenofos in combination with selenium treated group showed apparent reduction of caspase-3 immunoreactivity to be more or less similar to the control group. In conclusion, selenium is a valuable cytoprotective which reduced the oxidative stress toxicity induced by Profenofos in the reproductive system of male and female as well as liver and kidney albino rabbits.

Cardioprotective Effect of Selenium Against Cyclophosphamide-Induced Cardiotoxicity in Rats.

The objective of this study is to evaluate the possible protective effects of selenium (Se) against cyclophosphamide (CP)-induced acute cardiotoxicity in rats. A total of 42 male Spraque-Dawley rats were divided into six groups (n=7). Rats in the first group were served as control. Rats in the second group received CP (150mg/kg) at the sixth day of experiment. Animals in the third and fourth groups were treated with only 0.5 and 1mg/kg Se respectively for six consecutive days. Rats in the fifth and sixth groups received respective Se doses (0.5 or 1mg/kg) for 6days and then a single dose of CP administered on the sixth day. On day 7, the animals were sacrificed; blood samples were collected to measure malondialdehyde (MDA), glutathione (GSH), lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), and ischemia-modified albumin (IMA) levels. Heart tissues were processed routinely and tissue sections were stained with H+E for light microscopic examination. In the CP-treated rats MDA, LDH, CK-MB, and IMA serum levels increased, while GSH levels decreased. Microscopic evaluation showed that tissue damage was conspicuously lower in CP plus Se groups. Moreover, 1mg/kg Se was more protective than 0.5mg/kg Se as indicated by histopathological and biochemical values. In conclusion, Se is suggested to be a potential candidate to ameliorate CP-induced cardiotoxicity which may be related to its antioxidant activity.

Protective Effect of Selenium Against Cisplatin-Induced Ototoxicity in an Experimental Design.

Cisplatin is an effective chemotherapeutic agent in the treatment of several types of malignant solid tumors but its clinical use is associated with ototoxicity. In the present study, we investigated the effect of selenium administration on lipid peroxidation (malondialdehyde [MDA]) and cisplatin-induced ototoxicity in rats. Healthy wistar albino rats (n = 21) were randomly divided into 3 groups: control (C), cisplatin (Cis), cisplatin and selenium (Cis+Se). Cisplatin was administered for 3 days to Cis and Cis+Se groups. Cis+Se group received selenium 5 days before cisplatin injection and continued for 11 consecutive days. Hearing thresholds and lipid peroxidation (MDA) levels of the rats were recorded before injections and at the end of experimental protocol. The cochleas of animals were harvested for histologic and immunuhistochemical examinations. In biochemichal analyses, pretreatment with selenium prevented the elevation of MDA levels in Cis+Se group rats. Moreover, animals in Cis+Se group had better hearing threshold levels than animals in cis group. Samples obtained from the animals in Cis group revealed extensive loss of the normal microarchitecture of the organ of Corti. On the other hand, animals in Cis+Se group exhibited a preservation of the morphology of the organ of Corti and outer hair cells. In the immunohistochemical examinations of cochlear tissues stained with anti-caspase-3, a higher degree of immunopositivity was found in the Cis group. When Cis+Se group and Cis group were compared, significantly less immunopositivity occurred in the Cis+Se group (P < 0.05). Thus, it appears that pretreatment with selenium may reduce cisplatin-induced ototoxicity in rats.

Protective effects of Selenium and/or Melatonin against Cadmium Chloride induced Chromosomal aberrations in Swiss Albino mice Mus musculus BALB/c

The present study was aimed to investigate the protective role of selenium and melatonin with concentration (0.2 mg /kg b.wt./day) for selenium and (2.5 mg/kg b. wt./day) for melatonin. The doses were administered for five weeks five day per week against the genotoxic effect of orally given Cadmium chloride (1mg/kg b.wt. /day) to male albino mice for five weeks (five day per week). Thirty five male albino mice were divided into seven groups; each group contained five mice. Chromosomal studies in bone marrow cells were used as parameters in this evaluation. It was observed that the administration of Cadmium chloride generally produced more chromosomal aberrations such as (gap, break, ring, dicentric, centric fusion, end to end association, aneuploidy and polyploidy) compared with control. Chromosomal aberrations were reduced in treatment with the antioxidants (Selenium, melatonin) and their combinations .Finally, it was concluded that selenium and melatonin can serve as possible anti-genotoxic agent against the clastogenic effect of Cadmium chloride.

In vitro effects of simultaneous exposure to platinum and cadmium on the activity of antioxidant enzymes and DNA damage and potential protective effects of selenium and zinc

Circulating platinum (Pt) is detectable in the blood of Pt-treated cancer patients for over a decade after the treatment. Prolonged exposure to Pt, in combination with adverse compounds from nutrition and lifestyle, such as cadmium (Cd), could increase the risk from second cancers. The aim of this study was to investigate the effects of simultaneous exposure to Cd- and Pt-compounds on oxidative and DNA damage and the possible protective effects of zinc (Zn) and selenium (Se). The aqueous solutions of PtCl4, CdCl2 × H2O, ZnCl2 and Na2SeO3 were added, alone or in combination, to whole blood and isolated erythrocytes to produce the final concentrations of 2000 μg/L of Pt, 8 μg/L of Cd, 100 μg/L of Se, and 1000 μg/L of Zn. The activity of copper, zinc-superoxide dismutase, glutathione peroxidase and glutathione in whole blood was determined after 1 h exposure in in vitro conditions. The induction of DNA strand-breaks in human peripheral blood leukocytes was determined with the alkaline comet assay after 24 h exposure. Exposure to Pt and/or Cd decreased the activities of antioxidant enzymes and elevated DNA damage compared to control. A statistically significant change in the activity of both enzymes and in the induction of DNA strand-breaks was observed in the cells treated with Pt + Cd combination, while the addition of Se and/or Zn resulted in partial recovery of these effects. The results indicate that combined exposure to Pt and Cd could disrupt antioxidant protection of the organism and increase DNA damage, whereas Se and Zn could partially ameliorate these harmful effects.

Absence of selenium protection against methylmercury toxicity in harbour seal leucocytes in vitro

Previous studies described high concentrations of mercury (Hg) and selenium (Se) in the blood of harbour seals, Phoca vitulina from the North Sea. In the present study, we evaluated the in vitro potential protective effects of sodium selenite (Na2SeO3) and selenomethionine (SeMet) on cell proliferation of harbour seal lymphocytes exposed to MeHgCl 0.75μM. In vitro exposure of ConA-stimulated T lymphocytes resulted in severe inhibition of DNA synthesis, likely linked to severe loss of mitochondrial membrane potential at 0.75μM. Neither selenite nor SeMet showed a protective effect against MeHg toxicity expressed at the T lymphocyte proliferation level for harbour seals. Selenite and SeMet did not show negative effects regarding lymphocyte proliferation and mitochondrial membrane potential.To conclude, our results clearly demonstrated that MeHg affected in vitro immune cells exposure with no protective effects of selenium at a molar ratio Hg:Se of 1:10 in harbour seals from the North Sea.

The Protective Effect of Selenium on Oxidative Stress Induced by Waterpipe (Narghile) Smoke in Lungs and Liver of Mice.

Waterpipe smoking is common in the Middle East populations and results in health problems. In this study, we investigated the effects of exposure of mice to waterpipe smoke on oxidative stress in lungs and liver and the effects of selenium administration before smoke exposure on the oxidative stress. Twenty-four mice were divided equally into four groups: (i) the control mice received no exposure or treatment; (ii) mice exposed to waterpipe smoke; (iii) mice received intraperitoneal injection of 0.59μg selenium/kg body weight as sodium selenite 15min before the exposure to waterpipe smoke; and (iv) mice received intraperitoneal injection of 1.78μg selenium/kg body weight as sodium selenite 15min before the exposure to waterpipe smoke. Mice were exposed to waterpipe smoke every other day for four times within 8 successive days. Malondialdehyde and nitric oxide levels were significantly higher in the lungs and liver, while the activities of superoxide dismutase, glutathione peroxidase-1, and catalase were significantly lower in the waterpipe smoke group when compared to control mice. Treating mice with 1.78μg selenium/kg body weight significantly restored the normal levels of these parameters. Histological examinations of lungs and liver confirmed the protective actions of selenium against the effects of exposure to waterpipe smoke. In conclusion, exposure of mice to waterpipe smoke-induced oxidative stress in lungs and liver. Administration of low level of selenium, 1.78μg selenium/kg body weight as sodium selenite, exerted protective effects against oxidative stress induced by exposure to waterpipe smoke.

A histological study on the possible protective effect of selenium against chromium-induced thyrotoxicity in adult male albino rats

Background Chromium is hazardous for animals and human beings. Hexavalent chromium is highly toxic to life forms because of its carcinogenic, neurotoxic, nephrotoxic, genotoxic, and immunotoxic effects. Selenium is known for its antioxidant role in living systems, and therefore it is considered an essential element for humans and animals. Aim The present work aims at investigating the possible protective effect of selenium against chromium-induced thyrotoxicity in adult male albino rats. Materials and methods A total of 120 adult male albino rats were divided into three equal groups. The control group was given a single dose of sterile PBS daily for five consecutive days; the chromium-treated group was given a single dose of potassium dichromate daily for five consecutive days; and the selenium–chromium-treated group was given a single dose of nanoselenium and a single dose of potassium dichromate daily for five consecutive days. The animals of all groups were sacrificed at the same time and their thyroid glands were rapidly dissected out. The specimens of each group were processed for light and electron microscopic, and immunohistochemical studies. They were stained with hematoxylin and eosin, toluidine blue, and inducible nitric oxide synthase for evaluating follicular epithelial cells. Quantitative morphometric, and statistical studies were performed. Results Manifestations of cytotoxicity were visible on light and electron microscopic studies in chromium-treated thyroid sections in the form of disorganized follicles of varying diameters, with a preponderance of smaller over larger follicles. The follicular epithelial cells appeared to be enlarged and had a vacuolated cytoplasm. In addition, irregular shrunken nuclei were noticed. The thyroid gland of selenium–chromium-treated animals showed a near-normal follicular structure. Conclusion Administration of selenium in response to an increased risk of exposure to chromium compounds may protect the human body against their harmful effects.

Protective effect of selenium and zinc against cadmium toxicity in SHSY-5Y neurons

Cadmium is a widespread heavy metal environmental toxicant and pollutant. Cadmium toxicity affects many tissues and organs including the central nervous system and cadmium exposure has been related to many neurodegenerative diseases (1). Cadmium-induced toxic effects include oxidative damage, apoptosis, interference with calcium/zinc-dependent mechanisms, inhibition of cellular respiratory processes and others, but the underlying mechanisms of cadmium neurotoxicity are not completely understood (2). On the other hand heavy metal toxicity can be counteracted by bioelements such as zinc, selenium and others mainly through the induction of metallothionein expression levels and other antioxidant pro-teins (3). Human neuroblastoma SHSY-5Y cell line, in both the undifferentiated and neuronal-like differentiated state, were used in this study to better elucidate the mechanisms un-derlying the protective effect of zinc and selenium against the cadmium neurotoxicity. Toxic effects of cadmium chloride (10 mM, 24h) observed by cell viability assay, western blot anal-ysis of Bax and Gap-43, and immunostaining of b3 tubulin and cytochrome c proteins, were reverted to control values by a 24h-pretreatment with zinc chloride (50 mM) both in undiffer-entiated and differentiated neurons. Interestingly, the reverting effect of a 24h-pretreatment with sodium selenite (100 nM) against cadmium toxicity, was observed only in undifferentiat-ed neurons. In conclusion we can hypothesize that in undifferentiated and differentiated SHSY-5Y neurons, the protective effects of zinc and selenium compounds against cadmium toxicity depend on the activation of partially common signalling pathways. Moreover sodium selenite dont exert a significant protective effect in differentiated SHSY-5Y demonstrating that the differentiated and undifferentiated phenotypes show different responses.

Impact of a Short – Term Malathion Exposure of Nile Tilapia, ( Oreochromis niloticus ): The Protective Role of Selenium

Malathion is an organophosphate pesticide widely used to control a variety of insects in agriculture. It can reach the aquatic ecosystems affecting non target organisms like fish. The purpose of this study was to determine LC50 of malathion and to investigate the possible protective effects of selenium on malathion-induced toxicity in Nile tilapia. The fish were exposed to sub lethal concentrations of malathion (1/2 and 1/4 LC50) for 15 days, and selenium (5.54 mg/kg of fish weight) was simultaneously administered. Blood and liver samples were collected at the end of the experiment. Biochemical parameters [serum glucose, cortisol, acetylcholinesterase (AchE)], haematological profiles [white blood cells (WBCs), red blood cells (RBCs) counts, haemoglobin (Hb) concentration, haematocrit (Ht) level], and oxidant/antioxidant statuses [lipid peroxidation (LPO) level, superoxide dismutase (SOD), glutathione-S-transferase (GST) and catalase (CAT) activities] were analysed. The findings of the present study revealed that short-term exposure to malathion at sub lethal concentrations induced biochemical and haematological alterations in Oreochromis niloticus and led to oxidative damage. Moreover, the administration of selenium considered as an effective way to counter the toxicity of malathion in tilapia fish.

Selenoprotein W was Correlated with the Protective Effect of Selenium on Chicken Myocardial Cells from Oxidative Damage.

Selenium (Se) mainly performs its function through Se-containing proteins. Selenoprotein W (SelW), one member of the selenoprotein family, plays important roles in the normal function of the heart. To investigate the possible relationship between Se and SelW for the regulation of oxidative damage in chicken embryo myocardial cells, we treated myocardial cells with Se and H2O2. Then, the levels of lactate dehydrogenase (LDH) and 3,4-methylenedioxyamphetamine in the culture media, levels of SelW, inflammatory genes NF-κB, tumor necrosis factor (TNF)-α, p53, and the cell cycle were analyzed. Furthermore, the correlation between SelW and the levels of these factors was determined. The results indicated that Se treatment increased the expression of SelW (P<0.05) and caused a downregulation of p53, NF-κB, and TNF-α (P<0.05). In contrast, H2O2 increased the expression of p53, NF-κB, TNF-α, and LDH (P<0.05) and induced early cell apoptosis, which was alleviated by treatment with Se. In addition, SelW had a positive correlation with the levels of inflammatory genes investigated. Taken together, our findings suggested that SelW is sensitive to Se levels and oxidative stress, and may play a role in the protective function of Se against oxidative damage and inflammation in chicken myocardial cells.

Protective effects of selenium on cadmium neurotoxicity

Prolonged exposure to Cadmium may cause serious toxic effects due to its accu- mulation on both central and peripheral nervous systems. Cadmium could be uptak- en from the nasal mucosa via the olfactory pathways and gain direct access into the nervous system circumventing the blood-brain barrier. However, mechanisms under- lying the cadmium uptake and neurotoxicity remain not completely understood. Oxidative damage, interference with calcium-, copper- and zinc-dependent processes, dysregulation of cell repair mechanisms, estrogen-like effects, and epigenetic modifi- cations may be considered mechanisms for cadmium-induced neurotoxicity [1]. Our previous data demonstrated that zinc chloride counteracts the toxic effects of cadmium chloride (CdCl2) on human neurons in vitro [2]. Thus, in this study we evaluate the efficacy of Sodium Selenite (Na2SeO3) in preventing and/or counteracting the damages induced by exposure to cadmium chloride on a human neuronal cell line. In this study we treated SH-SY5Y human neurons with different sub-toxic concentrations of CdCl2 for 24 h with and without a 24 h pre-treatment with Na2SeO3. Cell viability, morphological modifications, and protein expression of specific neuronal plasticity and apoptosis (Gap43 and caspase 3) markers were evaluated. Our results suggest that toxic effects of CdCl2 can be prevented and reverted by Na2SeO3 suggesting a role for selenium compounds in protecting neuronal cells and rebuilding the complex network connections.