Role of beta-carotene in ameliorating the cadmium-induced oxidative stress in rat brain and testis

The role of oxidative stress in chronic cadmium (Cd) toxicity and its prevention by cotreatment with beta-carotene was investigated. Adult male rats were intragastrically administered 2 mg CdCl2/kg body weight three times a week intragastrically for 3 and 6 weeks. Brain and testicular thiobarbituric acid reactive substances (TBARS) was elevated after 3 and 6 weeks of Cd administration, indicating increased lipid peroxidation (LPO) and oxidative stress. Cellular damage was indicated by inhibition of adenosine triphosphatase (ATPase) activity and increased lactate dehydrogenase (LDH) activity in brain and testicular tissues. Chronic Cd administration resulted in a decline in glutathione (GSH) content and a decrease of superoxide dismutase (SOD) and glutathione S-transferase (GST) activity in both organs. Administration of beta-carotene (250 IU/kg i.g.) concurrent with Cd ameliorated Cd-induced LPO. The brain and testicular antioxidants, SOD, GST, and GSH, decreased by Cd alone, were restored by beta-carotene cotreatment. Concurrent treatment with beta-carotene also ameliorated the decrease in ATPase activity and the increase in LDH activity in brain and testis of Cd-treated rats, indicating a prophylactic action of beta-carotene on Cd toxicity. Therefore, the results indicate that the nutritional antioxidant beta-carotene ameliorated oxidative stress and the loss of cellular antioxidants and suggest that beta-carotene may control Cd-induced brain and testicular toxicity.     

Zinc protection against cadmium-induced infertility in female rats. Effect of zinc and cadmium on the progesterone production of cultured granulosa cells

Adult female rats were treated subcutaneously (sc) with zinc chloride (ZnCl, 10 or 20 mg kg body weight, bw) four times during two ovarian cycles. The third injection was accompanied by cadmium chloride (CdCl) administration sc (2.5, 5 and 10 mg kg bw). The fourth zinc (Zn) treatment was followed by mating.ZnCl (20 mg kg) itself impaired fertility by 20%, while CdCl dose-dependently blocked the receptivity of female rats. In combination with 2.5 and 5 mg kg CdCl the metal salts decreased fertility in an additive fashion, whereas at the highest CdCl dose (10 mg kg) a marked ameliorating effect of ZnCl (10 and 20 mg kg) on cadmium (Cd)-caused sterility was observed.In the pregnant animals apart from the higher Cd-induced blood progesterone levels and reduced body weight gain of dams, no significant treatment-related maternal and fetal effects could be observed. ZnCl (10 to 80 m) and CdCl (10 to 80 m) were added to the culture medium of ovarian granulosa cells. CdCl suppressed follicle-stimulating-hormone- (FSH-) and cAMP-stimulated progesterone accumulation. No protective effect of Zn against Cd-induced drop in progesterone production could be seen, while Zn by itself induced a significant increase in FSH-supported progesterone synthesis.In conclusion, while Zn protected against Cd-induced sterility in vivo, it failed to counteract the direct effect of Cd on steroid biosynthesis. The data indicate that Zn protection does not take place at the level of ovary. Moreover, Zn and Cd seem to affect FSH-stimulated progesterone production by different mechanisms.     

Effect of Physalis peruviana L. on Cadmium-Induced Testicular Toxicity in Rats

Cadmium (Cd) stimulates the production of reactive oxygen species and causes tissue damage. We investigated here the protective effect of Physalis peruviana L. (family Solanaceae) against cadmium-induced testes toxicity in rats. Twenty-eight Wistar albino rats were used. They were divided into four groups (n?=?7). Group 1 was used as control. Group 2 was intraperitoneally injected with 6.5 mg/kg body weight (bwt) of cadmium chloride for 5 days. Group 3 was orally treated with 200 mg/kg bwt of methanolic extract of physalis (MEPh). Group 4 was pretreated with MEPh before cadmium for 5 days. Changes in body and testes weights were determined. Oxidative stress markers, antioxidant enzymes, and testosterone level were measured. Histopathological changes of testes were examined, and the immunohistochemical staining for the proapoptotic (caspase-3) protein was performed. The injection of cadmium caused a significant decrease in body weight, while a significant increase in testes weight and testes weight index was observed. Pretreatment with MEPh was associated with significant reduction in the toxic effects of Cd as shown by reduced testicular levels of malondialdehyde, nitric oxide, and caspase-3 expression and increased glutathione content, and the activities of superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase, and testosterone were also increased. Testicular histopathology showed that Cd produced an extensive germ cell apoptosis, and the pretreatment of MEPh in Cd-treated rats significantly reduced Cd-induced testicular damage. On the basis of the above results, it can be hypothesized that P. peruviana L. has a protective effect against cadmium-induced testicular oxidative stress and apoptosis in the rat.     

The Retention of Cadmium and Selenium Influence in Fowl and Chickens of F1 Generation

The retention of cadmium and selenium influence on Cd retention in the muscle, liver and kidneys of hens, chickens and in eggs was studied. Cadmium (Cd) as cadmium chloride (CdCl(2)) and selenium (Se) as sodium selenite (Na(2)SeO(3)) were added to feed at dosages: group 0-control, group 1-20 mg/kg Cd, group 2-30 mg/kg Cd + 4 mg/kg Se. The birds were exposed to Cd for 8 weeks. Cadmium level in hens and cocks was found highest in the kidneys, followed by the liver and muscle. Se supplementation resulted in Cd increase in the muscle tissue and in the reduction of Cd content in the liver and in significant decrease in the kidneys (p < 0.05). A higher Cd level in the yolk and lower in the white was noted in both experimental groups. Nonsignificant increase of Cd in eggs was noted in experimental groups with Se supplementation. Level of cadmium in organs of 7-day-old chicks hatched from Cd-treated hens in both experimental groups was low but the tendency to accumulate preferentially the Cd in the liver and kidneys was recorded. Supplementation of selenium in hens and cocks was not reflected in the decrease of Cd in these two organs of F(1) chickens but was reflected in increase in the muscle. In spite of relatively high Cd levels in the organs of layers no layer-egg-chickens transfer was observed. It was confirm that kidneys and liver are organs more attacked by dietary cadmium than muscle. Supplementation of low dose of Se resulted in decrease of cadmium deposition in analyzed organs.     

Dithiocarbamates and prevention of cadmium teratogenesis in the hamster

Certain dithiocarbamates (DTC) have been reported to protect against cadmium (Cd)-induced lethality and to decrease Cd body burden. The present study evaluated the influence of sodium N-benzyl-D-glucamine dithiocarbamate, sodium N-di(hydroxyethyl)amine dithiocarbamate, sodium 4-carboxyamidopiperidine-N-dithiocarbamate, and sodium N-methyl-D-glucamine dithiocarbamate on Cd-induced teratogenesis in the hamster. When given as a single ip injection at 2.2 mmol/kg 15 min prior to iv CdCl2 (2 mg/kg), all of the DTC afforded significant protection against Cd-induced developmental toxicity and reduced kidney [Cd] in the dam. Maternal liver [Cd] was reduced with the glucamine and dihydroxyethyl amine analogs, but treatment with the piperidine failed to influence hepatic [Cd]. Pretreatment of the dams with DTC 24 hr prior to Cd challenge failed to protect against Cd-induced embryotoxicity, and provided minimal, if any, reduction in renal or hepatic [Cd]. Pretreatment with the N-methyl-D-glucamine congener 24 hr prior to Cd exposure increased embryolethality. The dose-time relationships found here suggest that pharmacologically effective levels of these DTC decline within 24 hr of treatment and that induction of metallothionein does not play a major role in DTC antagonism of Cd poisoning.     

Effects of Cadmium Chloride and Sodium Selenite Alone or in Combination on the Liver of Male Sprague–Dawley Rats Assessed by Different Assays

This study assessed the impact of either cadmium chloride (Cd) or sodium selenite (Se) alone or in combination on male Sprague–Dawley rats. For this purpose, body and liver weights, comet and TUNEL assays, histological analysis and levels of lipid peroxidation and antioxidants in liver were determined in four groups of male Sprague–Dawley rats. The rats were given subcutaneous doses of 1 mg/kg body weight (BW) of either normal saline (control = Ct) or Cd or Se or Cd plus Se (Cd + Se) on alternate days for 4 weeks. The Cd group showed increased DNA damage, apoptosis and hepatic levels of lipid peroxidation and altered histology. Conversely, the antioxidant levels in this group were decreased as compared with the control group. The Se group also showed DNA damage, apoptosis and altered histology and reduced catalase activity, but it was less severe than the Cd group. In the Cd + Se group, ameliorating effects of Se on Cd-induced changes were observed. While the Se was able to curtail the toxic effect of Cd, the Cd or Se alone were genotoxic and cytotoxic for rats receiving a high pharmacological but non-fatal dose of 1 mg/kg BW.     

Protective influence of vitamin E on antioxidant defense system in the blood of rats treated with cadmium

The effects of acute exposure to cadmium (Cd) on the blood antioxidant defense system, lipid peroxide concentration and hematological parameters, as well as the possible protective role of vitamin E were studied. Male Wistar albino rats (3 months old) were treated with cadmium (0.4 mg Cd/kg b.m., i.p., 24 h before the experiment) or with vitamin E + Cd (20 IU Vit E/kg b.m., i.m., 48 h + 0.4 mg Cd/kg b.m., i.p., 24 h before the experiment). The hematological parameters were assessed: red blood cell counts, hematocrit value and hemoglobin concentration were significantly decreased in the blood of Cd-treated rats. Intoxication with cadmium was also followed by significantly increased lipid peroxide concentrations. We also observed increased activity of antioxidant defense enzymes: copper zinc containing superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase as well as concentrations of non-enzymatic components of antioxidant defense system: reduced glutathione, vitamin C and vitamin E. Pretreatment with vitamin E exhibited a protective role on the toxic effects of cadmium on the hematological values, lipid peroxide concentration as well as on enzymatic and non-enzymatic components of antioxidant defense system.     

Effect of Treatment with Cadmium on Structure-Function Relationships in Rat Liver Mitochondria: Studies on Oxidative Energy Metabolism and Lipid/Phospholipids Profiles

Effects of treatment with a single intraperitoneal injection of cadmium (Cd) on oxidative energy metabolism and lipid/phospholipid profiles of rat liver mitochondria were examined at the end of 1 week and 1 month. Following Cd treatment the body weight increased only in the 1 month group, whereas the liver weight increased in both groups. State 3 and 4 respiration rates in general decreased significantly, with the maximum effect being seen with succinate. The 1 week Cd group showed decreased respiratory activity with glutamate, pyruvate + malate, and succinate as the substrates. In the 1 month Cd-treated group respiration rates recovered with glutamate and pyruvate + malate but not with succinate. All cytochrome contents decreased in the 1 week Cd-treated group but recovered in the 1 month group. ATPase activity registered an increase in both Cd-treated groups. Dehydrogenase activities increased in the 1 week group but decreased in the 1 month Cd-treated group. The mitochondrial cholesterol content increased in the 1 week Cd-treated group. In the 1 week Cd-treated group the lysophospholipid (Lyso), sphingomyelin (SPM), and diphosphatidylglycerol (DPG) components increased. By contrast, the phosphatidylethanolamine (PE) component decreased. In the 1 month Cd-treated group the phosphatidylinositol, phosphatidylserine, and DPG components increased, whereas the Lyso, SPM, and phosphatidylcholine components decreased. The results demonstrate that single-dose Cd treatment can have adverse effects on liver mitochondrial oxidative energy metabolism and lipid/phosphopholipid profiles, which in turn can affect membrane structure-function relationships.     

Induction of necrosis in cadmium-induced hepatic oxidative stress and its prevention by the prophylactic properties of taurine

The present study has been carried out to investigate the protective role of taurine against cadmium (Cd)-induced oxidative impairment in murine liver. Oral administration of cadmium chloride (CdCl₂) at a dose of 4 mg/kg body weight for 6 days increased the accumulation of the Cd in the liver and diminished the liver weight to body weight ratio. The CdCl₂ altered the levels of intracellular trace elements, cofactors of various metalloenzymes and increased the activities of serum marker enzymes related to liver dysfunction. In addition, Cd intoxication also attenuated intracellular antioxidant power, the activities of antioxidant enzymes as well as the levels of cellular metabolites. Moreover, level of hepatic metallothionein, lipid peroxidation, protein carbonylation, DNA fragmentation, concentration of intracellular reactive oxygen species (ROS) and the activities of cytochrome P450s have been increased due to Cd toxicity. In addition to the oxidative impairments, Cd exposure caused hepatic cell death mainly via the necrotic pathway. Oral administration of taurine at a dose of 100 mg/kg body weight for 5 days prior to CdCl₂ intoxication prevented the alterations of all the toxic-induced hepatic damages. Histological studies also supported the beneficial role of taurine against Cd-induced hepatic damages. Combining all, results suggest that taurine could protect hepatic tissues against Cd-induced oxidative stress probably through its antioxidant activity.     

Hepatoprotective Potentials of Onion and Garlic Extracts on Cadmium-Induced Oxidative Damage in Rats

The hepatoprotective effect of onion and garlic extracts on cadmium (Cd)-induced oxidative damage in rats is reported. Control group received double-distilled water alone. Cd group was challenged with 3CdSO₄·8H₂O (as Cd; 1.5 mg/kg bw per day per oral) alone, while extract-treated groups were pretreated with varied doses of onion and/or garlic extract (0.5 and 1.0 ml/100 g bw per day per oral) for a week and thereafter co-treated with Cd (1.5 mg/kg bw per day per oral) for 3 weeks. Cd caused a marked (p?<?0.001) increase in the levels of lipid peroxidation and glutathione S-transferase, whereas glutathione, superoxide dismutase, and catalase levels were decreased in the liver. We also observed a decrease in hepatic activities of alanine transaminase (ALT), aspartate transaminase (AST), and alkaline phosphatase and a concomitant increase in the plasma activities of ALT and AST. Onion and garlic extracts significantly attenuated these adverse effects of Cd. Onion extract proffered a dose-dependent hepatoprotection. Our study showed that Cd-induced oxidative damage in rat liver is amenable to attenuation by high dose of onion and moderate dose of garlic extracts possibly via reduced lipid peroxidation and enhanced antioxidant defense system that is insufficient to prevent and protect Cd-induced hepatotoxicity.     

Effects of sodium N-methyl-N-dithiocarboxyglucamine on cadmium distribution and excretion

Sodium N-methyl-N-dithiocarboxyglucamine (MDCG) was evaluated for its efficacy in mobilizing and promoting excretion of metallothionein-bound 109Cd using mice which had received 0.03 mg of CdCl2 . 2 . 5H2O along with 1.0 muCi of 109CdCl2 three weeks earlier. The MDCG-induced change in the fecal excretion of Cd ranged from a 15-fold increase over the control rate at the lowest dose level used (2.2 mmol/kg; 684 mg/kg) up to a 72-fold increase at the highest dose (8.8 mmol/kg; 2736 mg/kg) following three daily injections. The latter treatment regimen resulted in a fecal excretion of almost 30% of the administered Cd over a 3-day period of observation. Urinary Cd excretion was insignificant in both the control and treated groups. The whole body burden of Cd was reduced by over 50% following seven thrice-weekly i.p. injections of MDCG at 8.8 mmol/kg. There was a 60-65% reduction in both the liver and kidney Cd levels following the same treatment regimen. Radioassay of ten other organs and tissues revealed only modest changes. Testicular Cd was decreased slightly at the highest dose level, and heart tissue from each treated group contained slightly more Cd than controls. Results indicated a rather marked specificity of MDCG in lowering the Cd content of two organs most susceptible to Cd-induced toxicity.     

Effects of Montmorillonite on Alleviating Dietary Cd-Induced Oxidative Damage in Carp (Carassius auratus)

The present study was designed to investigate the effects of montmorillonite (MMT) on dietary Cd-induced oxidative damage in liver and kidney of carp (Carassius auratus). One hundred eighty carp were randomly divided into four groups and fed with a basal diet, a basal diet supplemented with 0.5% MMT, Cd-comtaminated basal diet (120 mg Cd/kg dry weight) and Cd-contaminated basal diet supplemented with 0.5% MMT, respectively. After 60 days, fish were sacrificed to measure malondialdehyde (MDA) content and antioxidative indices in liver and kidney. The results showed that the exposure of carp to dietary Cd caused decreases in glutathione peroxidase activity, catalase activity, superoxide dismutase activity, glutathione content and total antioxidant capacity level, while MMT supplemented in diet compensated Cd-induced decreases in above antioxidant indices to some extent in liver and kidney. As compared with the control group, increases in MDA content were observed in both measured tissues of carp exposed to dietary Cd, while MDA content decreased in carp exposed to Cd-contaminated basal diet supplemented with MMT in comparison with the Cd-contaminated group. It was suggested that MMT, when co-administered with Cd in diet, could alleviate dietary Cd-induced oxidative damage in liver and kidney of carp.     

Influence of static magnetic field on cadmium toxicity: Study of oxidative stress and DNA damage in rat tissues

In the present study, we investigated the effect of co-exposure to static magnetic field (SMF) and cadmium (Cd) on the biochemical parameters, antioxidant enzymes activity and DNA damage in rat tissues. Animals were treated with cadmium (CdCl₂, 40 mg/L, per os) in drinking water during 4 weeks. Cd treatment induced an increase of plasma lactate dehydrogenase (LDH) and transaminases levels. Moreover, Cd treatment increased malondialdehyde (MDA) and 8-oxodGuo levels in rat tissues. However, the antioxidant enzymes activity such as the glutathione peroxidase (GPx), catalase (CAT) and the superoxide dismutase (SOD) were decreased in liver and kidney, while we noted a huge increase of hepatic and renal cadmium content. Interestingly, the combined effect of SMF (128mT, 1 h/day during 30 consecutive days) and Cd (40 mg/L, per os) decreased the GPx and CAT activities in liver compared to cadmium treated group. However, the association between SMF and Cd failed to alter transaminases, MDA and 8-oxodGuo concentration.

Cd treatment altered antioxidant enzymes and DNA in liver and kidney of rats. Moreover, SMF associated to Cd disrupt this antioxidant response in liver compared to Cd-treated rats.     

Effect of chronic cadmium exposure on antioxidant defense system in some tissues of rats: protective effect of selenium

The effects of selenium (Se) on antioxidant defense system in liver and kidneys of rats with cadmium (Cd)-induced toxicity were examined. Cd exposure (15 mg Cd/kg b.m./day as CdCl(2) for 4 weeks) resulted in increased lipid peroxidation (LP) in both organs (p<0.005 and p<0.01). Vitamin C (Vit C) was decreased in the liver (p<0.005), whereas vitamin E (Vit E) was increased in the liver and kidneys (p<0.005 and p<0.05) of Cd-exposed animals. Superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were decreased in both tissues (p<0.05 and p<0.005), whereas catalase (CAT) activity was decreased only in liver (p<0.005). Glutathione S-transferase (GST) increased in both tissues (p<0.005 and p<0.01). Treatment with Se (0.5 mg Se/kg b.m./day as Na(2)SeO(3) for 4 weeks) significantly increased liver and kidneys SOD and GSH-Px activities (p<0.05 to p<0.005), as well as CAT and GST activities only in the liver (p<0.01). In animals exposed to Se, both the concentrations of Vit C (p<0.01) and Vit E (p<0.005) were increased in both tissues. Co-treatment with Se resulted in reversal of oxidative stress with significant decline in analyzed tissues Cd burden. Our results show that Se may ameliorate Cd-induced oxidative stress by decreasing LP and altering antioxidant defense system in rat liver and kidneys and that Se demonstrates the protective effect from cadmium-induced oxidative damage.     

Modulation of acute cadmium toxicity by Emblica officinalis fruit in rat

The efficacy of Emblica officinalis in modifying the acute cytotoxicity of cadmium in male rats was evaluated. Oral administration of Emblica fruit juice (500 mg/kg, b.w.) for 8 days followed by a single toxic dose of Cd as CdCl2 (3 mg/kg,b.w. ip), considerably reduced the mortality in rats as well as prevented to some extent the cadmium induced histopathological damage in testis, liver and kidneys. Biochemical investigation also revealed reduced levels of Cd induced serum glutamate oxaloacetate transaminase, glutamate pyruvate transaminase and gamma glutamyltranspeptidase. The enhanced levels of Cd and lipid peroxidation in liver, kidney, and testes and metallothionein and total sulphydryl in liver and kidney by Cd were significantly reduced by Emblica pretreatment. These results suggest cytoprotective potential of Emblica fruit in acute cadmium toxicity which could be due to its multiple role in biological system.     

Lead and Cadmium Co-exposure Mediated Toxic Insults on Hepatic Steroid Metabolism and Antioxidant System of Adult Male Rats

The redox status and steroid metabolism of liver of adult male rat exposed to lead (Pb) and cadmium (Cd) either alone or in co-exposure (0.025 mg/kg body weight intraperitoneally/15 days) was studied. Pb and Cd significantly accumulated in the liver. The activity of steroid metabolizing enzymes 17-βhydroxysteroid oxidoreductase and uridine diphosphate–glucuronyltransferase were decreased in experimental animals. 17-β-Hydroxysteroid dehydrogenase was reduced to 33%, 38%, and 24% on treatment of Pb, Cd, and co-exposure (Pb + Cd). Furthermore, the activity of uridine diphosphate–glucuronosyltransferase was significantly reduced to 27% (Pb exposure), 36% (Cd exposure), and 25% (co-exposure of Pb + Cd). Cd exposure exhibited more toxic effect than Pb, while co-exposure demonstrated the least. The activities of antioxidant enzymes, superoxide dismutase, catalase, glutathione reductase, and glucose-6-phosphate dehydrogenase decreased and glutathione peroxidase increased in mitochondrial and post-mitochondrial fractions. The level of lipid peroxidation increased, and cellular glutathione concentration decreased. Hepatic DNA was decreased, whereas RNA content and the activity of alanine transaminase remained unchanged. Histological studies revealed that only Cd-exposed groups exhibited cytotoxic effect. These results suggest that when Pb and Cd are present together in similar concentrations, they exhibited relatively decreased toxic effect when compared to lead and cadmium in isolation with regard to decreased steroid metabolizing and antioxidant enzyme activities. This seems that the toxic effect of these metals is antagonized by co-exposure due to possible competition amongst Pb and Cd for hepatic accumulation.     

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.     

Influence of aqueous extract of Hibiscus sabdariffa L. petal on cadmium toxicity in rats

The effects of chronic exposure to cadmium (Cd) on some selected biochemical parameters, as well as the possible protective role of aqueous extracts of Hibiscus sabdariffa L petal were studied in 12-wk-old male Wistar albino rats. Exposure to Cd caused a significant increase in plasma l-alanine aminotransferases (ALT) only but with a corresponding decrease in liver l-alanine and l-aspartate aminotransferases (L-ALT, L-AST) when compared to the Cd-free control. Total superoxide dismutase activity was decreased in the liver, testis, and prostate of Cd-exposed rats, whereas malondialdehyde (MDA) concentrations were increased relative to the Cd-free control. The metal significantly increased prostatic acid phosphatase activity in the prostate, but decreased the body weight gain of the rats and organ/body weight ratio for prostate and testis compared to the Cd-free control. Pretreatment of rats with aqueous extract of H. sabdariffa resulted in significantly less hepatotoxicity than with Cd alone as measured by plasma ALT and liver ALT and AST activities. The extract also protected the rats against Cd-induced liver, prostate, and testis lipoperoxidation as evidenced by significantly reduced MDA values in these organs, as well as reduced prostatic acid phosphatase activity in the prostate, when compared to the Cd-only exposed rats. Also, when compared to the organ/body weight ratios obtained from rats exposed to Cd alone the prostate and testis were protected by the extract as shown by enhanced prostate/body weight and testis/body weight ratios of Cd- and extract-treated rats. These data suggest that H. sabdarrifa L might be protective in Cd toxicity.     

Selenium Supplementation Changes the Ion Profile in the Pancreas of Chickens Treated with Cadmium

Increasing evidence indicates that selenium (Se) could antagonize metal toxicity, including cadmium (Cd) toxicity. However, the effects of Se on Cd-induced changes in the ion profile in the pancreas of chickens have not been reported. In the present study, 128 Hy-Line brown laying chickens were divided into the control group, Se-treated group, Se/Cd-treated group, and Cd-treated group, and we detected the concentrations of 28 ions in the four groups by inductively coupled plasma mass spectrometry. In the Cd-treated group, the accumulation of Cd in the pancreas was 836.8 times higher that than in the control group (27,353.71 ppb/32.69 ppb). Meanwhile, the Ca, Ti, Fe, Mo, Li, Al, and Pb levels increased and the Cr, Mn, Ni, Cu, Zn, Se, Sr, and Sb levels decreased due to sub-chronic Cd poisoning. The Fe, Mo, Ba, and Pb levels decreased in the Se/Cd-treated group. Our findings suggest that Cd can accumulate in the chicken pancreas and affect the ion profiles, whereas Se can ameliorate the accumulation of Cd and change the ion profiles in the chicken pancreas.     

Effect of exposure of pregnant rats to cadmium on prenatal and postnatal development of the young

Cadmium chloride in doses of 2, 12 and 40 mg Cd/kg was administered per os to pregnant rats from the 7th to 16th day of pregnancy. In another experiment female rats were exposed to cadmium oxide at a concentration of 0.02 mg Cd/m3 or 0.16 mg Cd/m3 for 5 hours a day and 5 days weekly for a period of 5 months or 1 mg Cd/m3 for 4 months. The exposure was then continued during mating and from the 1st to 20th day of pregnancy. A decrease in fertility was only observed in females exposed by inhalation to cadmium oxide at a concentration of 1 mg Cd/m3, at which concentration cadmium exhibits a considerable toxic effect on the whole organism. The young of females orally treated with CdCl2 in a dose of 40 mg Cd/kg displayed congenital defects in the form of sirenomelia or amelia, as well as raised cadmium levels in tissues. A retardation of intrauterine development manifested by lower body weight and slowed down osteogenesis was observed in the other groups. A cadmium concentration increase was not found in the tissues of the young in these groups. Inhalation exposure to 0.16 mg Cd/m3 of females prior to and during pregnancy induced in their young a decrease in viability, lower body weight gain, prolongation of latency in the negative-geotaxis test, lower locomotor activity and deteriorated development of the conditioned-reflex response. The offspring of females exposed to 0.02 mg Cd/m3 displayed lowered locomotor activity and worsened consolidation of the conditioned-reflex response.