The effect of dietary selenium supplementation on cadmium absorption and retention in suckling rats

Selenium (Se) reduces cadmium (Cd) toxicity in adult animals, but its effects in newborn animals are still unknown. This study investigated Cd (as CdCl₂) absorption, distribution, and retention in suckling rats receiving oral Se supplementation (as Na₂SeO₃) in equimolar doses (8 μmol Cd and/or Se per kg b.w./day). Selenium was given either before and during Cd exposure (Se_pre + Cd group; pre-treatment group) or only during Cd exposure (Se + Cd group). Rats were treated from postnatal day (PND) 6–14 as follows: controls (H₂O, PND 6–14), Se (PND 10–14), Cd (PND 10–14), Se_pre + Cd (Se PND 6–14 + Cd PND 10–14) and Se + Cd (Se + Cd PND 10–14). Selenium supplementation, especially pre-treatment, decreased Cd levels in the blood, brain, liver and kidney of suckling rats. Selenium levels in plasma, brain, and kidney also decreased. These findings suggest that higher Se intake could efficiently reduce Cd retention during the suckling period.     

The ameliorative effect of fluoxetine on neuroinflammation induced by sleep deprivation

It is well known that sleep disorders are harmful to people's health and performance, and growing evidence suggests that sleep deprivation (SD ) can trigger neuroinflammation in the brain. The nucleotide‐binding domain and leucine‐rich repeat protein‐3 (NLRP 3) inflammasome is reported to be relevant to the neuroinflammation induced by SD , but the regulatory signaling that governs the NLRP 3 inflammasome in SD is still unknown. Meanwhile, whether the regulatory action of antidepressants in astrocytes could affect the neuroinflammation induced by SD also remains obscure. In this study, we were the first to discover that the antidepressant fluoxetine, a type of specific serotonin reuptake inhibitor widely used in clinical practice, could suppress the neuroinflammation and neuronal apoptosis induced by SD . The main findings from this study are as follows: (i) SD stimulated the expression of activated NLRP 3 inflammasomes and the maturation of IL ‐1β/18 via suppressing the phosphorylation of STAT 3 in astrocytes; (ii) SD decreased the activation of AKT and stimulated the phosphorylation of GSK ‐3β, which inhibited the phosphorylation of STAT 3; (iii) the NLRP 3 inflammasome expression stimulated by SD was partly mediated by the P2X7 receptor; (iv) an agonist of STAT 3 could significantly abolish the expression of NLRP 3 inflammasomes induced by an agonist of the P2X7 receptor in primary cultured astrocytes; (v) the administration of fluoxetine could reverse the stimulation of NLRP 3 inflammasome expression and function by SD through elevating the activation of STAT 3. In conclusion, our present research suggests the promising possibility that fluoxetine could ameliorate the neuronal impairment induced by SD .

     

Morphological and functional alterations induced in trout intestine by dietary cadmium and lead

Effects of oral administration of lead and cadmium on structure and function of trout intestine were investigated in Salmo gairdneri. Fish were fed either cadmium (5 mg kg*¹ fish per day) or lead (10 mg kg⁻¹ fish p er day) and sacrificed after a 15 or 30 day treatment.
Levels of cadmium and lead in kidney, liver and spleen were significantly increased by the 15th day of treatment.
Following both cadmium and lead treatment, morphological observations showed an increased mucous cell activity, a disruption of intestinal brush border and an increased renewal rate of absorptive cells.
Influx (J_ms), outflux (J_sm) of chlorine and sodium ion and net fluxes were measured on perfused intestinal segments and ouabain-sensitive sodium, potassium-ATPase (Na, K-ATPase) activity was determined on intestinal scrapings. Cadmium did not alter either sodium chlorine transepithelial fluxes or sodium, potassium-ATPase activity, but lead did. In the middle intestine, lead modified significantly transepithelial sodium and chlorine fluxes (J_ms Na: 3.21 ± 0.34 to 1.79 ± 0.29 and J_ms Cl: 3.32 ± 0.34 to 1.86 ± 0.22μmol h⁻¹ cm⁻², n = 6) after 30-day diet. J_net remain unchanged and Na, K-ATPase activity decreased. In the posterior intestine, lead altered only J_ms Na (1.95 ± 0.31 to 0.37 ± 0.09μmol h⁻¹ cm⁻²) and J_ms Cl. Consequently J_nes were also decreased.
So, although both cadmium and lead induce morphological disorders in the middle and in the posterior intestine of the trout, they have different effects on the absorption mechanisms of ions.     

Studies on the toxic effect of cadmium in the rat. I. Testicular changes induced by a single subcutaneous injection of cadmium chloride.

Adult male rats of Wistar strain were subcutaneously injected with a single dose of 0.025 mM CdCl2/kg body weight. The autopsies were performed 2 and 12 weeks post cadmium injection. Experimental animals showed a normal gain of body weight while a marked lowering of the testes weight was observed. The lowering of testes weight of cadmium treated rats occured mainly due to the necrosis of seminiferous tubules, volume of which is markedly lower if compared to intact control rats. After 2 weeks of experiment a marked enlargement of the interstitial gland of the testis occured while after 12 weeks the gland is markedly lower if compared to control rats and to rats studied 2 weeks post cadmium injection. Histochemical reactions for lactic, succinic, alpha-glycerophosphate and 3beta-hydroxy steroid dehydrogenases, NADH tetrazolium reductase, acid phosphatase and nonspecific esterases showed for irreversible necrotic changes of seminiferous tubules of cadmium treated rats while the damage to interstitial gland is only temporary.     

Effect of dietary copper on selenium toxicity in Fischer 344 rats

The purpose of this study was to investigate the ameliorating effects of dietary copper supplementation on selenium toxicity. Nine groups (n = 6) of weanling Fischer 344 female rats were randomly assigned to treatment groups and fed diets containing nontoxic levels of copper as CuCl2 and/or selenium as selenite or selenocystamine. Weight gain, liver and spleen weights, plasma lipid peroxidation, and liver selenium and copper content were analyzed after the 6-wk treatment period. Concentrations of up to 10 times the daily lethal dose of dietary selenium were well tolerated in rats supplemented with dietary copper. As the dietary level of selenium was increased, the ratio of selenium to copper measured in the liver decreased. In the groups of rats in which dietary copper supplementation was absent and dietary selenium was supplemented, copper stores in the liver remained unchanged from control values. Copper's protective effects from dietary selenium toxicity may come from the formation of a copper-selenide complex that renders both selenium and copper metabolically unavailable and nontoxic.     

The protective effect of selenium inorganic forms against cadmium and silver toxicity in mycelia of Pleurotus ostreatus

The effect of two inorganic selenium forms has been investigated in the mycelia of Pleurotus ostreatus exposed to cadmium and silver salts in the shaken cultures. The degree of toxicity was assessed by the determination of malondialdehyde (MDA; a common biomarker of lipid peroxidation). The mycelia were exposed to one element form (up to 5 mg l⁻¹) and also to the following combinations: cadmium(II) + selenium(IV); cadmium(II) + selenium(VI); silver(I) + selenium(IV); silver(I) + selenium(VI). The concentrations of cadmium, silver, selenium, and MDA were assessed in the mixed cytosol and cell membrane fractions (CCM). A positive correlation between MDA and cadmium was found in the CCM (β = 0.7775, P = 0.0001), whereas the effect of silver was less significant (β = 0.4642, P = 0.039). These results indicate that silver(I) and cadmium(II) have different capacities to induce lipid peroxidation in P. ostreatus. The protective role of selenium against metal-induced oxidative damage was found to be dependent on the oxidation state of the element form in the growth medium. The strongest beneficial effect was observed in mycelia exposed to cadmium(II) + selenium(IV) (inverse correlation between MDA and selenium in the CCM: β = −0.7129, P = 0.009) and it has been ascribed to a lower incorporation of the toxic metal and/or to possible intracellular interaction between selenium and cadmium. Under exposure to silver(I), the protective effect of selenium(IV) was less noticeable (correlation between MDA and selenium in the CCM; β = −0.6068, P = 0.036); in the presence of selenium(VI), no beneficial effect was observed.     

Inhibition of glutathione reductase by cadmium ion in some rabbit tissues and the protective role of dietary selenium

This study is aimed at investigating the inhibitory effect of cadmium ion on glutathione reductase activity of rabbit brain and liver and the relationship of this effect with dietary selenium. For this purpose, one group of New Zealand rabbits were fed a selenium-deficient diet, another group was fed a selenium-rich diet, and the control group was fed a normal diet. The brain and liver tissues of these groups were investigated for the in vitro inhibitory effects of Cd²⁺ on glutathione reductase activity. For liver, the percentage inhibition of glutathione reductase by 40 nmol/mg protein of Cd²⁺ was similar for selenium-deficient and control groups, but significantly lower in the selenium-rich group. For brain tissues, there was no difference with respect to cadmium inhibition of glutathione reductase in all three groups.     

The initial pathogenesis of cadmium induced renal toxicity

The novel application of magic angle spinning 1H NMR spectroscopy, coupled with pattern recognition techniques, has identified biochemical changes in lipid and glutamate metabolism that precede classical nephrotoxicity. These changes occurred in the bank vole (Clethrionomys glareolus) after chronic dosing, at a low level of exposure and at a renal Cd(2+) concentration (8.4 microgram/g dry wt) that was nearly two orders of magnitude below the WHO critical organ concentration (200 microg/g wet wt). These early stage effects of Cd(2+) on the biochemistry of renal tissue may reflect adaptation mechanisms to the toxic insult or the preliminary stages of the toxicological cascade.     

Serum metabonomics analysis of quercetin against the toxicity induced by cadmium in rats

This study aimed to investigate the protective effect of quercetin against the toxicity induced by chronic exposure to low levels of cadmium in rats by an ultra performance liquid chromatography mass spectrometer. Rats were randomly divided into six groups as follows: control group (C), low dose of quercetin group (Q1: 10 mg/kg·bw), high dose of quercetin group (Q2: 50 mg/kg·bw), cadmium chloride group (D), low dose of quercetin plus cadmium chloride group (DQ1), and high dose of quercetin plus cadmium chloride group (DQ2). Cadmium chloride (CdCl₂) was administered to rats by drinking water ad libitum in a concentration of 40 mg/L. The final amount of CdCl₂ ingested was estimated from the water consumption data to be 4.85, 4.91, and 4.89 mg/kg·bw/day, for D, DQ1, and DQ2 groups, respectively. After a 12‐week treatment, the serum samples of rats were collected for metabonomics analysis. Ten potential biomarkers were identified for which intensities were significantly increased or reduced as a result of the treatment. These metabolites included isorhamnetin 4′‐O‐glucuronide, 3‐indolepropionic acid, tetracosahexaenoic acid, lysophosphatidylcholine (LysoPC) (20:5), lysoPC (18:3), lysophosphatidylethanolamine (LysoPE) (20:5/0:0), bicyclo‐prostaglandin E2, sulpholithocholylglycine, lithocholyltaurine, and glycocholic acid. Results indicated that quercetin exerted a protective effect against cadmium‐induced toxicity by regulating lipid and amino acid metabolism, enhancing the antioxidant defense system and protecting liver and kidney function.     

Chemopreventive mechanism of action by oxidative stress and toxicity induced surface decorated selenium nanoparticles

BackgroundScientists are working on creating novel materials that can help in the treatment of diverse cancer-related diseases having trademark highlights like the target siting, specificity, improved therapeutic index of radiotherapy and chemotherapeutic treatments. The utilization of novel nanomaterials which are surface adorned with drugs or natural compounds can be used in diverse medical applications and helps in setting up a new platform for its improvement in the chemotherapeutic potentiality. One such nanomaterial is the trace element selenium in its nanoparticulate form that has been proved to be a potential chemotherapeutic agent recently.MethodsThe English language papers were gathered from electronic databases like Sciencedirect, Pub Med, Google Scholar and Scopus, the papers are published from 2001 to 2019.ResultsIn the initial phase, approximately 200 papers were searched upon, out of which 118 articles were included after screening and critical reviewing. The information included was also tabulated for better knowledge and easy read. These articles contain information on the nanotechnology, inflammation, cancer and selenium as nanoparticles.ConclusionThe overview of the paper explains the enhancement of potentiality of anticancer drugs or phytochemicals which restricts its utilization in chemotherapeutic applications by the encapsulation or adsorption of them on selenium nanoparticles proven to accelerate the anticancerous properties with better results when compared with individual components. SeNPs (selenium nanoparticles) have demonstrated chemotherapeutic activity due to pro-oxidant property, where the anti-oxidant enzymes are stimulated to produce reactive active species, which induces oxidative stress, followed by activation of the apoptotic signalling pathway, cell cycle arrest, mitochondrial dysfunction and other pathways that ultimately lead to cell death. Selenium in nanoparticulate form can be used as a micronutrient to human health, thereby having low toxicity, can easily be degraded and also has good biocompatibility.     

Influence of dietary selenium on metabolism of cadmium and mercury in reproductive tissues of rats

Dietary selenium supplementation for rats resulted in a greater deposition of ¹⁰⁹Cd in testis, but caused decreased deposition of the isotope in seminal vesicles, epididymis and prostate gland. In contrast, dietary selenium caused increased deposition of ²⁰³Hg in seminal vesicles and prostate gland but drastically reduced the levels of this radioisotope in testis and epididymis. Selenium diverted the binding of ¹⁰⁹Cd in cytosols in testis, seminal vesicles, epididymis and prostate gland, but had minimal effects on the binding of ²⁰³Hg in these reproductive organs. Selenium deficiency caused increased excretion of ¹⁰⁹Cd in feces and urine, and increased excretion of ²⁰³Hg in urine of rats. The biological half-lives of the two radioisotopes in the −Se and +Se rats were calculated to be, respectively, 202 and 219 days for ¹⁰⁹Cd, and 2 and 6 days for ²⁰³Hg.     

Bioremediation of cadmium induced renal toxicity in Rattus norvegicus by medicinal plant Catharanthus roseus

Cadmium is the second most hazardous metals with bio-concentration factor (BCF)?>?100 Although WHO permitted cadmium concentration in drinking water is 0.005?mg/L, yet the reality is far above to this limit because of industrial utility of this metal. Oral exposure of cadmium to human results in dreadful symptoms of metabolic disorders especially in liver and kidneys. Endogenous protection could be supported by some exogenous herbal supplement (viz., Catharanthus roseus in this case) to overcome the toxic effects. Present Study has been designed to find out the functional renal changes under the effect of cadmium and Catharanthus roseus in the model organism albino rats. Cadmium significantly (p?>?0.01) increases the level of nitrogenous waste (Urea, BUN, Uric Acid and Creatinin), while decreases the serum protein profile in acute and sub-acute sets. Urea concentration of control ranged from 16.56 to 17.72?mg/dl while that of Group-B and D were 19.84 to 20.87?mg/dl and 17.56 to 17.59?mg/dl respectively. Similarly uric acid concentration ranged in control form 6.98 to 8.01?mg/dl in group-B from 7.58 to 10.25?mg/dl, in Group-D 8.02 to 8.59?mg/dl respectively. Creatinin concentration ranged in control 0.57 to 0.65?mg/dl, in group-B 0.97 to 1.02?mg/dl, in group-D – 0.95 to 0.98?mg/dl respectively.These results might be due to altered filtration rate of kidney because of protein disruption. The studies conclude the efficient nephro-protection offered by Catharanthus roseus extract against Cadmium toxicity.     

The role of organic selenium in cadmium toxicity: effects on broiler performance and health status

This work was part of a project designed to assess whether organic selenium (Se) can protect against the toxic effects of cadmium (Cd). A total of 300 1-day-old, as hatched, broilers were randomly distributed in four dietary treatments with five replicate pens per treatment. In T1 treatment, broilers were fed a diet with 0.3 mg/kg added Se, as Se-yeast, without added Cd; in T2, broilers were fed a diet with 0.3 mg/kg Se and 10 mg/kg Cd; in T3, broilers were fed a diet with 0.3 mg/kg Se and 100 mg/kg of Cd; and in T4 treatment broilers were fed a diet with 3 mg/kg Se and 100 mg/kg Cd. The Cd was added to diets T2, T3 and T4 as CdCl₂. On the 4th and 6th week, two broilers per replicate pen were killed in order to obtain whole blood, liver, kidney and breast samples. Body mass, feed conversion ratio and mortality were assessed and haematological analyses were performed. Se and Cd levels in tissues were analysed by inductively coupled plasma mass spectrometry. Broilers supplemented with 0.3 mg/kg Se can tolerate low levels of Cd added to the diets, as there were no significant negative effects on the examined performance parameters, whereas addition of excess Cd led to an impairment of broilers’ performance. Mortality of broilers did not differ between the four dietary treatments at any interval point or the whole period. The examined haematological parameters such as haematocrit, total blood protein concentration, and leukocytes types ranged within physiological values, revealing no negative health effects after simultaneous Cd and Se addition. The present study indicated that Se can help against the negative effects of Cd, but cannot counteract all of its negative effects.     

Testicular toxicity induced by dietary cadmium is associated with decreased testicular zinc and increased hepatic and renal metallothionein and zinc in the bank vole <Emphasis Type="Italic">(Clethrionomys glareolus)</Emphasis>

Mechanism of testicular toxicity induced by dietary cadmium (Cd) has been less investigated than that following acute Cd injection. In the present study we characterized testicular injury in a small rodent, the bank vole, exposed subchronically to dietary Cd in a quantity of 0.9 mol/g, and determined the importance of some factors (Cd accumulation, metallothionein (MT), oxidative stress, and zinc (Zn)) in the injury. Dietary Cd induced moderate histopathological changes (hemorrhage in interstitium, necrosis and apoptosis in seminiferous tubule epithelium) in young (1 month old) bank voles fed, for 6 weeks, Fe-adequate (1.1–1.4 mol/g) and Fe-enriched (4.5–4.8 mol/g) diets. In contrast, adult (5 months old) bank voles appeared to be resistant to the toxic effects of dietary Cd, despite the fact that testicular Cd contents were higher and MT levels lower than those in the young animals. The Cd-induced histopathological changes and apoptosis were accompanied by increased testicular lipid peroxidation, decreased testicular Zn concentration and elevated levels of hepatic and renal MT and Zn. Supplemental dietary Zn (1.7–1.8 mol/g) prevented the Cd-induced testicular Zn depletion and injury. The data indicate that dietary Cd produces testicular lesions indirectly, through decreasing testicular Zn, which seems to be due to the sequestration of this element by the Cd-induced hepatic and renal MT.     

Protection by metallothionein against cadmium toxicity

1. The protective effect against Cd toxicity of prior exposure to Cd or Zn solutions at low concentration was studied. 2. Carp were bred in tap water (A), 1 ppm Cd solution (B) and 5 ppm Zn solution (C) for 14 days and then transferred into 15 ppm Cd solution. The survival ratio of carp decreased in the order: (C):(B):(A). 3. Binding capacity of Cd to high molecular and metallothionein fractions in the cytoplasmic solutions of the hepato-pancreas was studied and the binding capacity to the metallothionein fraction was stronger than that to the high molecular fraction. The authors recognized that Zn in the metallothionein fraction is substituted by Cd.     

Changes in wheat plastid membrane properties induced by cadmium and selenium in presence/absence of 2,4-dichlorophenoxyacetic acid

The aim of the work was to recognize the effect of cadmium (Cd) and selenium (Se) onto properties of plastid lipid membranes. Plastids were isolated from wheat calli cultured during 2 weeks on Murashige–Skoog media with presence/absence of 2,4-dichlorophenoxyacetic acid. Plastids obtained in presence of 2,4-D represented an earlier developmental stage in comparison to those, got in absence of 2,4-D, which reached a pre-chloroplast stage. The studied metals were introduced to culture media separately (2 μM Na₂SeO₄ or 800 μM CdCl₂) or together (Se + Cd). The changes of following properties of plastid envelope membrane caused by both metals were measured: composition of main lipid fractions, their fatty acid saturation, membrane fluidity, lipid peroxidation and membrane zeta potential. Results of experiments led to the conclusion that galactolipid component plays a predominant role in modification of plastid membrane properties responding to Cd and Se addition. It was shown that galactolipid protecting reaction to Cd toxic action can consists in increased plastid envelope membrane stiffness. The presence of hormone (2,4-D) and Se did not counterbalance Cd toxic effects (at least under concentration level applied in the experiments). Se applied separately can probably stimulate plastid/chloroplast transformation in wheat cells by increasing a galactolipid unsaturation degree. The zeta potentials seem to be important physicochemical parameter in determination of properties of membranes exposed to metal stress conditions.     

Effect of spirulina and Liv-52 on cadmium induced toxicity in albino rats

Oral administration of cadmium (6mg/kg body weight/day) as cadmium chloride (CdCl2) for 30 days resulted in a significant increase in thiobarbituric acid reactive substances (TBARS) level and a decrease in the levels of copper, zinc, iron, selenium, glutathione, superoxide dismutase, catalase, glutathione peroxidase when compared to normal control. Administration of either Liv-52 alone or in combination with spirulina produced a well pronounced protective effect in respect to these parameters in cadmium intoxicated rats. The protective effect of spirulina and Liv-52 in respect to biochemical changes were also confirmed by histopathological study in the liver and kidney sections.     

Arsenic-induced toxicity and the ameliorative role of antioxidants and natural compounds

Arsenic (As) poisoning has proven to be a major threat worldwide because of its toxic effects on the human body. As toxicity through drinking water is a global health concern. The toxicity of As is known to affect the liver, kidney, lungs, muscles, cardiovascular system, and nervous system and can even induce diabetes. Further As can cause skin lesions leading to notable diseases in the skin like Bowen's disease. Chronic exposure to As has caused many tragedies in Eastern, and several Southeast Asian and Latin American countries. Long-term exposure to As makes it an immediate threat that should be dealt with as a priority, and one of the ways to handle it may be with the use of antioxidants. In this review, we have discussed the natural and anthropogenic sources of As, its metabolism, pathophysiology, and mechanism of toxicity. Besides, we have also discussed some of the synthetic chelators and the ameliorative role of antioxidants and natural compounds in reducing As toxicity.