Atorvastatin prevents cadmium-induced renal toxicity in a rat model.

In many industrial processes, worker exposure to cadmium causes kidney damage; thus, protection against cadmium toxicity is important in workplace health. Cadmium toxicity involves oxidative stress by increasing the levels of reactive oxygen species. Statins have shown antioxidant effects that might prevent this increase in oxidative stress. We investigated the potential effects of atorvastatin pretreatment in protecting experimental rats against kidney toxicity caused by cadmium. Experiments were performed on 56 adult male Wistar rats (200 ± 20 g), randomly assigned to eight groups. Atorvastatin was administered by oral gavage for 15 days at 20 mg/kg/day, starting 7 days before cadmium chloride intra-peritoneal administration (at 1, 2, and 3 mg/kg) for 8 days. On day 16, blood samples were collected, and kidneys were excised to evaluate the biochemical and histopathological changes. Cadmium chloride significantly increased malondialdehyde, serum creatinine, blood urea nitrogen, and decreased superoxide dismutase, glutathione, and glutathione peroxidase levels. Pre-administration of rats with atorvastatin at a dose of 20 mg/kg decreased blood urea nitrogen, creatinine, and lipid peroxidation, increased the activities of antioxidant enzymes, and prevented changes in physiological variables compared with animals that were not pretreated. Atorvastatin pretreatment prevented kidney damage following exposure to toxic doses of cadmium. In conclusion, atorvastatin pretreatment in rats with cadmium chloride-induced kidney toxicity could reduce oxidative stress by changing biochemical functions and thereby decreasing damage to kidney tissue.

Musa sp. Leaves Extract Ameliorates the Hepato-Renal Toxicities Induced by Cadmium in Mice.

Heavy metals intoxication causes several health problems that necessitate finding new protective and therapeutic approaches. This study aimed to evaluate the impact of Musa sp. leaves extract (MLE) on hepato-renal toxicities induced by cadmium (Cd) in male mice. The phytochemical screening, metal chelating activity (MCA), and the median lethal dose (LD50) of MLE were determined. Fifty CD-1 male mice were used and intraperitoneally (i.p.) injected with MLE (1000 to 5000 mg/kg b.wt) for MLE LD50 determination. Another 50 mice were used for evaluating the effect of MLE on Cd toxicity. Blood samples were collected for hematological, liver, and kidney functions assessments. Liver tissue homogenates were used for determination of oxidant/antioxidant parameters. Liver and kidney tissues were harvested for histopathological and molecular investigations. MLE showed potent in vitro antioxidant activities. The MCA and LD50 of the MLE were 75 µg/mL and 3000 mg/kg b.wt, respectively. MLE showed beneficial therapeutic activity against hepato-renal toxicities in Cd-intoxicated mice, evidenced by improving the hematological, biochemical, histopathological, and molecular alterations.

Protective Role of the Essential Trace Elements in the Obviation of Cadmium Toxicity: Glimpses of Mechanisms.

Cadmium (Cd) is toxic non-essential heavy metal that precipitates adverse health effects in humans and animals. Chelation therapy, the typical treatment for cadmium toxicity, has certain safety and efficacy issues to treat long term cadmium toxicity, in particular. Recent studies have shown that essential trace elements can play important roles in obviating experimental Cd toxicity. This study organizes and reviews the prototypical evidences of the protective effects of essential trace elements against Cd toxicity in animals and attempts to point out the underlying mechanisms. Zinc, selenium, iron, and combinations thereof are reported to be active. The major mechanisms elucidated inter alia are-induction of metallothionein (MT) synthesis and Cd-MT binding (for zinc), modulation of oxidative stress and apoptosis, interference in cadmium absorption and accumulation from body-thereby maintenance of essential metal homeostasis and cytoprotection. Based on the findings, essential trace elements can be recommended for the susceptible population. The application of these trace elements appears beneficial for both the prevention and remediation of long-term Cd toxicity operative via multiple mechanisms with no or minimal adverse effects as compared to the conventional chelation therapy.

In Vivo Attenuation of Alcohol- and Cadmium Chloride-Induced Testicular Toxicity Modulated by Silymarin in Male Wistar Rat.

The aim of the study is to investigate the in vivo attenuation of alcohol- and cadmium chloride-induced testicular toxicity modulated by Silymarin in male Wistar rats. A total of fifty-six (56) Wistar rats were used for this study and they were randomized into seven (7) groups of eight (8) rats each. Group 1 was control rats; Groups 2-7 served as the experimental groups. After 6 weeks treatment duration, the rats were euthanized, semen was collected for semen analysis, blood samples for testosterone, and FSH and LH assay determination, and left testes was harvested for histological analysis. One-way ANOVA was used to compare means at p-level < 0.05 was considered significant. Findings from this study have shown that alcohol and cadmium chloride adversely affected semen parameters, testosterone, and FSH and LH hormone milieu. Data also showed that Silymarin administration attenuated the adverse effect of alcohol and cadmium chloride on semen quality and hormones associated with reproductive functions. Hence, Silymarin mopped the effect of in vivo attenuation of alcohol and cadmium chloride testicular damage. The findings of this study have further established that alcohol and cadmium chloride adversely affected semen parameters, testicular alterations, and serum hormonal milieu. However, the effect was more significantly deleterious in rats exposed to cadmium chloride when compared to rats exposed to alcohol, subsequently alcohol- and cadmium chloride-induced degeneration of testicular tissues. Furthermore, Silymarin administration attenuated the adverse effect of alcohol on semen quality and hormones associated with reproductive functions.

The Impact of a Polyphenol-Rich Extract from the Berries of Aronia melanocarpa L. on Collagen Metabolism in the Liver: A Study in an In Vivo Model of Human Environmental Exposure to Cadmium.

This study examined whether a polyphenol-rich extract from the berries of Aronia melanocarpa L. (AE; chokeberries) may protect from the impact of cadmium (Cd) on the metabolism of collagen in the liver. The study was conducted in an experimental model (rats that were fed a diet containing 1 or 5 mg Cd/kg for 3-24 months) of human exposure to this xenobiotic during a lifetime. The concentration of total collagen and the expression of collagen types I and III at the mRNA and protein levels, as well as the concentrations of matrix metalloproteinases (MMP-1 and MMP-2) and their tissue inhibitors (TIMP-1 and TIMP-2), were assayed. The administration of Cd and/or AE had only a slight and temporary impact on the concentration of total collagen in the liver. The supplementation with AE significantly prevented Cd-mediated changes in the expression of collagen types I and III at the mRNA and protein levels and their ratio (collagen III/collagen I), as well as a rise in the concentrations of MMPs and TIMPs in this organ. The results allow the conclusion that the intake of chokeberry products in the case of Cd intoxication may be effective in prevention from this xenobiotic-induced disturbance in collagen homeostasis in the liver.

The neuroprotective effect of curcumin against Cd-induced neurotoxicity and hippocampal neurogenesis promotion through CREB-BDNF signaling pathway.

Heavy metal neurotoxicity is one of the major challenges in today's era due to the large scale and widespread mechanisation of the production. However, the causative factors responsible for neurotoxicity are neither known nor do we have the availability of therapeutic approaches to deal with it. One of the major causative agents of neurotoxicity is a non-essential transition heavy metal, Cadmium (Cd), that reaches the central nervous system (CNS) through the nasal mucosa and olfactory pathway causing adverse structural and functional effects. In this study, we explored the neuroprotective efficacy of plant derived Curcumin which is reported to have pleiotropic biological activity including anti-oxidant, anti-inflammatory, anti-apoptotic, anti-carcinogenic and anti-angiogenic effects. Four different concentrations of curcumin (20, 40, 80 and 160 mg/kg of the body weight) were used to assess the behavioural, biochemical, hippocampal proteins (BDNF, CREB, DCX and Synapsin II) and histological changes in Swiss Albino mice that were pre-treated with Cd (2.5 mg/kg). The findings showed that Cd exposure led to the behavioural impairment through oxidative stress, reduction of hippocampal neurogenesis associated proteins, and degeneration of CA3 and cortical neurons. However, treatment of different curcumin concentrations had effectively restored the behavioural changes in Cd-exposed mice through regulation of oxidative stress and up-regulation of hippocampal proteins in a dose-dependent manner. Significantly, a dose of 160 mg/kg body weight was found to be glaringly effective. From this study, we infer that curcumin reverses the adverse effects of neurotoxicity induced by Cd and promotes neurogenesis.

The Role of Probiotics in the Amelioration of Cadmium Toxicity.

Cadmium is extremely toxic heavy metal, and there is no specific, safe, and efficacious therapeutic management of cadmium toxicity. Scientific literature reveals several probiotic microorganisms which alleviate experimentally induced cadmium toxicity in animals. The present review attempts to collate the experimental studies on probiotics and probiotic-derived natural products with cadmium toxicity ameliorative effects. Literature survey revealed that seven (7) types of probiotic microorganisms exhibited significant protection from cadmium toxicity in experimental pre-clinical studies. Clinical study with significant outcome was not found in literature. From the outcomes of the pre-clinical studies, it appears that probiotics have the prospect for alleviation and treatment of cadmium toxicity.

Glutamate alleviates cadmium toxicity in rice via suppressing cadmium uptake and translocation.

Cadmium (Cd), a naturally occurring heavy metal, is toxic to animals and plants. Minimization of Cd in rice grain is important to human health since rice is the main source of Cd intake for human populations feeding on it as staple food. Glutamate (Glu) is reportedly involved in plant abiotic stress responses, whereas the underlying molecular mechanism remains poorly understood. In this study, we showed that supplement of Glu, but not glutamine, significantly alleviated Cd toxicity in hydroponically grown rice plants. Cd accumulation was reduced by 44.1% and 65.6% in root and shoot of rice plants respectively, after Glu supplementation (3 mM). Glu supplement restored chlorophyll biosynthesis and significantly ameliorated Cd-induced oxidative stress with reduced levels of H2O2, 1O2, MDA, and increased activities of major anti-oxidant enzymes, catalase, peroxidase and glutathione S-transferase. Levels of stress-associated free amino acids proline, arginine and γ-aminobutyric acid were also reduced after Glu supplement. We further demonstrated that Glu supplement suppressed the Cd-induced expression of metal transporter genes OsNramp1, OsNramp5, OsIRT1, OsIRT2, OsHMA2 and OsHMA3 in roots of Cd-treated plants. Taken together, our results suggest that Glu supplement could alleviate Cd toxicity in rice by suppressing Cd uptake and translocation.

Back to Nucleus: Combating with Cadmium Toxicity Using Nrf2 Signaling Pathway as a Promising Therapeutic Target.

There are concerns about the spread of heavy metals in the environment, and human activities are one of the most important factors in their spread. These agents have the high half-life resulting in their persistence in the environment. So, prevention of their spread is the first step. However, heavy metals are an inevitable part of modern and industrial life and they are applied in different fields. Cadmium is one of the heavy metals which has high carcinogenesis ability. Industrial waste, vehicle emissions, paints, and fertilizers are ways of exposing human to cadmium. This potentially toxic agent harmfully affects the various organs and systems of body such as the liver, kidney, brain, and cardiovascular system. Oxidative stress is one of the most important pathways of cadmium toxicity. So, improving the antioxidant defense system can be considered as a potential target. On the other hand, the Nrf2 signaling pathway involves improving the antioxidant capacity by promoting the activity of antioxidant enzymes such as catalase and superoxide dismutase. At the present review, we demonstrate how Nrf2 signaling pathway can be modulated to diminish the cadmium toxicity.

Possible prophylactic effect of omega-3 fatty acids on cadmium-induced neurotoxicity in rats' brains.

Cadmium (Cd) has long been noted to induce neurodegenerative disorders. Therefore, this study aimed to assess the toxicological impact of Cd on rat brains and evaluate the possible ameliorative impact of omega-3 fatty acids as a protective agent of nervous system. Rats were divided into four groups: group I supplemented orally with saline; group II intoxicated with CdCl2 (5 mg/kg b.w. orally), and groups III and VI supplemented with omega-3 (100 mg/kg b.w. orally) simultaneously or before CdCl2 administration, respectively. Cd intoxication induced biochemical and histopathological disturbances in treated rats. Omega-3 fatty acid considerably improved the Cd-associated biochemical changes, reduced the elevation of lipid peroxidation, and normalized the Cd impact on the levels of superoxide dismutase, catalase, glutathione-S-transferases, 8-hydroxydeoxyguanosine, heatshock protein70, nuclear factor-κB, and interferon-γ as well as of neuronal enzymes such as acetylecholinesterase and monoamine oxidase within the brains of treated rats. Additionally, histological findings supported the results that Cd treatment-induced neurodegenerative changes and that polyunsaturated fatty acids act as antioxidants and neuroprotective agents against Cd toxicity. Co-treatment with omega-3 fatty acid was more beneficial than pretreatment. Thus, omega-3 fatty acid should be included in diet to prevent or suppress neurodegenerative disorders caused by continuous exposure to Cd.

Royal jelly attenuates cadmium-induced nephrotoxicity in male mice.

Cadmium exposure induces nephrotoxicity by mediating oxidative stress, inflammation, and apoptosis. The purpose of this study was to examine the protective effect of royal jelly on Cd-induced nephrotoxicity. Adult male mice were distributed randomly into 4 clusters: untreated, royal jelly-treated (85 mg/kg, oral), CdCl2-treated (6.5 mg/kg, intraperitoneal), and pretreated with royal jelly (85 mg/kg) 2 h before CdCl2 injection (6.5 mg/kg, intraperitoneal) for seven consecutive days. Cd concentration in the renal tissue and absolute kidney weight of the Cd-treated mice were significantly higher than those of control group. The levels of kidney function markers, kidney injury molecules-1 (KIM-1), metallothionein, lipid peroxidation, nitric oxide, tumor necrosis factor-α, interleukin-1ß, and the apoptosis regulators Bax and caspases-3 also increased significantly in the renal tissue of Cd-treated mice, whereas the levels of glutathione, antioxidant enzyme activities, and the apoptosis inhibitor Bcl-2 were significantly reduced in the renal tissue of Cd-treated group. Histopathological studies showed vacuolation and congested glomeruli in the kidney tissue of Cd-treated mice. However, all aforementioned Cd-induced changes were attenuated by pretreatment with royal jelly. We therefore concluded that royal jelly attenuated Cd-induced nephrotoxicity and it is suggested that this nephroprotective effect could be linked to its ability to promote the nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant responsive element (ARE) pathway.

The potential modulatory role of herbal additives against Cd toxicity in human, animal, and poultry: a review.

Cadmium (Cd) is a heavy and toxic metal and easily absorbed by animals and plants; subsequently, it is an environmental risk factor with several toxic effects in humans and animals. The main pathway of human or animal exposure to Cd is through its ingestion by water or food and by particles or fume inhalation during industrial processes. With continuous exposure to small levels of cadmium, it is being deposited in different tissues day after day, causing toxic effects on the liver, kidney, and testes. Long-term exposure to this toxic metal resulted in inflammatory infiltration, necrosis of hepatocytes, degenerative changes in testis tissues, reduction in spermatocytes, degeneration in renal tubules, and hypertrophy of renal epithelium. Therefore, we need an effective treatment to overcome cadmium poisoning. Thus, in the current review, we try to provide compiled reports and summarize information about the toxicological effects of Cd in human, animals, and poultry. This review also provides updated information about the protective actions of herbs and herbal extracts and their role as an effective strategy in reducing or preventing serious health problems and tissue damage in response to Cd toxicity.

Protective Effect of Ganoderma Triterpenoids on Cadmium-Induced Testicular Toxicity in Chickens.

Studies have shown that cadmium can cause chicken testicular damage, but a protective effect of Ganoderma triterpenoids on cadmium-induced testicular damage in chickens has not yet been reported. The present study was designed to research the protective effect of Ganoderma triterpenoids on cadmium-induced testicular damage in chicken. Eighty healthy 7-day-old Hyline egg laying chickens were randomly divided into four groups with 20 in each group. The control group was fed with normal full-fodder, the model group was fed with normal full-fodder with 140 mg/kg of CdCl2, the Ganoderma triterpenoid treatment group was fed with a full-fodder diet containing 140 mg/kg of CdCl2 and 0.5 mL of Ganoderma triterpenoid solution (20 mg/mL), and the Ganoderma triterpenoid group was fed normal full-fodder and 0.5 mL of Ganoderma triterpenoid solution (20 mg/mL) gavage. The chickens were euthanized at 20, 40, and 60 days, respectively, and the testes were harvested. The changes of cadmium contents, the antioxidant enzymes (superoxide dismutase (SOD), glutathione peroxidase (GSH-Px)), peroxide (malondialdehyde (MDA)), inflammatory factors (interleukin (IL)-1ß, IL-6, and tumor necrosis factor alpha (TNF-α)), and apoptosis-related proteins (Bax, Bcl-2, and Caspase-3) were detected. The pathological sections of the testes were made at the same time. The results suggested that Ganoderma triterpenoids could reduce the accumulation of cadmium in testis tissue; reduce the content of IL-1ß, IL-6, and TNF-α in cadmium poisoning testis; significantly increase the activity of SOD and GSH-Px; decrease the content of MDA; regulate the expression of Bax, Caspase-3, and Bcl-2; and reduce the damage of testicular tissue. The results showed that Ganoderma triterpenoids have a protective effect on cadmium-induced testicular injury in chicken.

The Effects of a Workplace Health Promotion Program to Decrease Cadmium Exposure Levels in Nickel-Cadmium Battery Workers.

OBJECTIVE: Cadmium exposure is a common problem in the production of nickel-cadmium batteries. However, keeping the respective legislative occupational and safety policies is essential, but there are problems with compliance. We analysed the effect of strategies to increase compliance with precautions during 20132015 on 59 workers at a nickel-cadmium battery factory. MATERIAL AND METHODS: A health promotion program was implemented in two phases. The first phase included comprehensive education on the importance of appropriate behaviour and changes to the sanitation program. The second phase included renovation of sanitary facilities and modernization of the air exhaust ventilation. RESULTS: The initial median cadmium urinary level in workers was 1.9 µg/g creatinine. After the first phase of interventions, levels dropped to 1.0 µg/g creatinine. After the second phase no significant further decrease was observed. CONCLUSION: Comprehensive education and changes in the sanitation program were able to halve cadmium levels and can be considered a useful and cost-effective preventive tool.

Effects of coenzyme Q10 supplementation on oxidative stress and antioxidant enzyme activity in glazers with occupational cadmium exposure: A randomized, double-blind, placebo-controlled crossover clinical trial.

TRIAL REGISTRATION:: Iranian Registry of Clinical Trials Registration Number: IRCT2016061228407N1 ( www.who.int/ictrp/network/irct/en/ ).

Cadmium induced damage in Wistar rats, ameliorative potentials of progesterone.

Asides the increased human exposure to Cadmium containing products; the adverse effects of Cadmium on human health is further exacerbated by its toxicity at low dosage, long biologic half-life and low rate of excretion from the body. This study investigated the protective potential of progesterone on cadmium-induced damage in Wistar rats. Adult male Wistar rats received CdCl2 once daily for 21 days. Progesterone was given 30 min. after administration of CdCl2 while 3 other groups were given distilled water, CdCl2 and progesterone alone. Blood samples were collected from the animals for the determination of liver function and antioxidant status while the liver, kidney, cerebellar and hippocampal tissues were excised and fixed in Neutral buffered formalin for histopathological studies. While Cadmium caused changes in liver function parameters which were indicative of oxidative stress, pre-treatment with progesterone caused restoration to values which were non-significant to the control. Similar findings were made for G6PD, GSH, SOD, CAT and MDA. Histopathology revealed tissue damage in the Cd treated group; this was attenuated by prior treatment with progesterone. Progesterone ameliorated the free radical induced oxidative stress and tissue injury arising from exposure to Cadmium; attention should be given to its antioxidant role in Cadmium toxicity.

Selenium and zinc: Two key players against cadmium-induced neuronal toxicity.

Cadmium (Cd), a worldwide occupational pollutant, is an extremely toxic heavy metal, capable of damaging several organs, including the brain. Its toxicity has been related to neurodegenerative diseases such as Alzheimer's and Parkinson's diseases. The neurotoxic potential of Cd has been attributed to the changes induced in the brain enzyme network involved in counteracting oxidative stress. On the other hand, it is also known that trace elements, such as zinc (Zn) and selenium (Se), required for optimal brain functions, appears to have beneficial effects on the prevention of Cd intoxication. Based on this protective effect of Zn and Se, we aimed to investigate whether these elements could protect neuronal cells from Cd-induced excitotoxicity. The experiments, firstly carried out on SH-SY5Y catecholaminergic neuroblastoma cell line, demonstrated that the treatment with 10 µM cadmium chloride (CdCl2) for 24 h caused significant modifications both in terms of oxidative stress and neuronal sprouting, triggered by endoplasmic reticulum (ER) stress. The evaluation of the effectiveness of 50 µM of zinc chloride (ZnCl2) and 100 nM sodium selenite (Na2SeO3) treatments showed that both elements were able to attenuate the Cd-dependent neurotoxicity. However, considering that following induction with retinoic acid (RA), the neuroblastoma cell line undergoes differentiation into a cholinergic neurons, our second aim was to verify the zinc and selenium efficacy also in this neuronal phenotype. Our data clearly demonstrated that, while zinc played a crucial role on neuroprotection against Cd-induced neurotoxicity independently from the cellular phenotype, selenium is ineffective in differentiated cholinergic cells, supporting the notion that the molecular events occurring in differentiated SH-SY5Y cells are critical for the response to specific stimuli.

Alleviation of cadmium-induced oxidative stress by trehalose via inhibiting the Nrf2-Keap1 signaling pathway in primary rat proximal tubular cells.

Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor that regulates a cluster of oxidative stress-inducible genes in cells. Here, we aimed to investigate whether trehalose (Tre) protects primary rat proximal tubular (rPT) cells against cadmium (Cd)-induced oxidative stress via Nrf2 antioxidant pathway. Data showed that Tre treatment inhibited Nrf2 nuclear translocation and restored the decline in Kelch-like ECH-associated protein 1 (Keap1) protein level in Cd-exposed rPT cells. Moreover, Cd-activated Nrf2 target genes, including phase II detoxifying enzymes, that is, NAD(P)H quinone oxidoreductase 1 and heme oxygenase-1, direct antioxidant proteins, that is, glutathione peroxidase, superoxide dismutase, catalase, and glutathione biosynthesis-related proteins, that is, glutamatecysteine ligase catalytic subunit, glutamate cysteine ligase modifier subunit, and glutathione reductase, were all downregulated by co-treatment with Tre. Collectively, these findings demonstrate that Tre treatment alleviates Cd-induced oxidative stress in rPT cells by inhibiting the Nrf2-Keap1 signaling pathway.

The effect of tannic acid on bone mechanical and geometric properties, bone density, and trabecular histomorphometry as well as the morphology of articular and growth cartilages in rats co-exposed to cadmium and lead is dose dependent.

Cadmium (Cd) and lead (Pb) are toxic elements that accumulate to the largest extent in bones. Rats were used to investigate whether tannic acid (TA; 0.5%, 1.0%, 1.5%. 2.0%, or 2.5%) would have a protective effect on the structure and properties of bones in the case of exposure to Cd and Pb (diet: 7 mg Cd/kg and 50 mg Pb/kg) for 6 weeks. The effects of administration of TA in Cd- and Pb-poisoned rats on bone characteristics and the morphology of articular and growth cartilages were determined. All the rats administered Cd and Pb had an enhanced Cd and Pb concentration in blood plasma and bone and reduced bone Ca content irrespective of the TA administration. Cd and Pb alone reduced the mechanical endurance and histomorphometric parameters of trabecular bone and the thickness of the growth plate and articular cartilage. Tannic acid improved cancellous bone parameters in the rat exposed to Cd and Pb. A diet rich in TA improved articular cartilage constituents in heavy metal-poisoned rats. These results suggest that alimentary TA supplementation can counteract in a dose-dependent manner some of the destructive changes evoked by Cd and Pb possibly by reducing the exposure.

Neuro- and nephrotoxicity of subchronic cadmium chloride exposure and the potential chemoprotective effects of selenium nanoparticles.

Cadmium (Cd) exposure leads to production of reactive oxygen species (ROS), which are associated with Cd-induced neurotoxicity and nephrotoxicity. Selenium nanoparticles (Se-NPs) have high bioavailability and antioxidant activities so it attracted wide spread attention. The present study examined the possible ameliorative effect of Se-NPs with diameters of 3-5 nm and 10-20 nm against cadmium chloride (CdCl2)-induced neuro- and nephrotoxicity in rats. Rats were treated with Se-NPs (0 or 0.5 mg/kg BW, s.c.) one hour prior to the CdCl2 (0 or 5 mg/kg BW, p.o.). Pretreatment with Se-NPs significantly decreased CdCl2-induced elevation of serum kidney and brain damage biomarkers; lipid peroxidation; the percent of DNA fragmentation and nearly normalized the activity of acetylcholinesterase (AchE) and significantly increased the activity and expression of antioxidant biomarkers in the RNA and protein levels. Se-NPs also attenuated CdCl2-induced upregulation of kidney and brain pro-apoptotic B-cell CLL/lymphoma 2 associated X (Bax) RNA and protein levels with preventing the increased body burden of Cd and the altered Fe and Cu homeostasis. Histopathological analysis confirmed the biochemical and molecular outcomes. Our data stated that Se-NPs appear to be effective in ameliorating the adverse neurological and nephrotoxic effects induced by CdCl2 partially through the scavenging of free radicals, metal ion chelation, averting apoptosis and altering the cell-protective pathways. The results indicated that Se-NPs could potentially included as an additive to Cd-based industries to control Cd-induced brain and renal injury.