Chromium in the Diet of Dairy Calves: Benefits for Growth Performance, Feed Efficiency, Digestibility, and Health.

Chromium (Cr) is a mineral that helps animals subjected to stressful conditions. The suckling period is characterized by several stressful episodes, particularly during the first hours after birth and at weaning. There is little consumption of concentrate by calves in the first weeks of life; consequently, consuming any supplement added to feed would be negligible. Thus, the hypothesis was that the calves would take it in earlier if Cr were consumed in a milk replacer instead. Therefore, our study aimed to determine whether including organic Cr in calf feed (via milk replacer or concentrate) during the suckling phase would improve calf health and growth performance. Twenty-four male Holstein calves with an average age of 8 ± 4 days and 39.8 ± 6.9 kg average body weight were used. Calves were randomly divided into three groups: (a) Chromium-Milk (CR-M), receiving 4 mg Cr/animal/day via milk replacer during the 60 experimental days of suckling (n = 8); (b) Chromium-Concentrate (CR-C), receiving 4 mg Cr/animal/day via concentrate (n = 8); (c) Control (C), animals that did not receive Chromium (n = 8). The experiment lasted 75 days, divided into two well-defined stages: suckling (1-60 days) and weaning (61-75 days). Body weight weekly, daily feed intake, and blood samples taken every two weeks during the experiment were evaluated. At the end of the experiment, the apparent digestibility evaluation was carried out, with the results of weight and consumption carried out, and a feed efficiency analysis was carried out. It was observed that the inclusion of organic Cr (regardless of whether it was milk or concentrate) increased body weight gain (kg) for the CR-C group: 41.8 kg, CR-M: 40.4 kg compared to the C: 34.2 kg (p = 0.01). The protein digestibility was higher in the CR-M group (52%, p = 0.05). Cr consumption increased Cr concentrations in the serum of the calves and was higher in the first week in the animals in the CR-M group. This did not happen for the C group; however, with higher concentrate consumption, Cr concentrations increased and remained high until the end of the experiment. Glucose concentrations were higher in the groups that consumed Cr. Total protein concentrations were higher in the CR-M and CR-C groups than in group C. Immunoglobulin A concentrations were higher in groups CR-C and CR-M than in group C (days 40 and 60). In conclusion, the adding Cr to calf feed improves their health, indirectly favors growth performance, and increases protein digestibility.

Addition of chromium propionate in dog food: metabolic, immunological, and oxidative effects.

Chromium is a trace element essential in metabolising carbohydrates, lipids, and proteins and is involved in other biological functions. Therefore, this study determined whether chromium propionate supplementation in dogs improves haematologic, metabolic, immune/inflammatory, and antioxidant biomarkers. A commercial product (Labex® Chromium) containing 0.4% chromium was used at 500 g/ton of food, which provided an additional calculated amount of 2 mg of chromium per kg of food. We used ten beagles divided into two treatments: the chromium group (supplemented with 0.380 mg of chromium/dog/day; T-CHR) and the control group comprised dogs fed a basal diet (no chromium supplementation). The experiment included two periods of 28 days, with an interval of 15 days, i.e. the dogs in the control group in the first period were in the chromium group in the second period (all dogs underwent all treatments in a crossover design). Dogs supplemented with chromium had higher serum mineral levels on days 14 and 28 (P ≤ 0.001). The group in the chromium group showed significantly higher numbers of total leukocytes and lymphocytes and concentrations of total protein, globulin, thio-proteins, and catalase activity in blood than the control group. Serum urea concentrations and TBARS (lipid peroxidation) were lower (P ≤ 0.05) in the chromium group. Tendencies towards lower concentrations of reactive oxygen species were observed on day 28 in the T-CHR group (P = 0.10). Chromium supplementation increased the concentration of cytokines in serum (tumour necrosis factor-alpha [TNF-α], IFN-γ, and IL-10) and C-reactive protein (P ≤ 0.05). Dogs in the chromium group had higher gamma globulin concentrations than controls (P ≤ 0.001). These findings suggest that supplementation with chromium propionate (2 mg/kg) in food positivity modulates metabolic, antioxidant, and immune indicators in dogs.

Effects of biocholine powder supplementation in ewe lambs: Growth, rumen fermentation, antioxidant status, and metabolism.

The objective of this study was to evaluate the effects of biocholine powder (BP) added to the concentrate of ewe lambs on growth, rumen fermentation, antioxidant status, and metabolism. Forty-eight Lacaune lambs were divided 3 treatments: T0, T4, and T8, representing 0, 4, and 8 g of BP per animal/day added to the concentrate, respectively. The T4 and T8 lambs had greater average daily gain from d 0-75 (0.22, 0.25, and 0.26 kg/d for T0, T4 and T8, respectively). T4 and T8 lambs had higher methylene blue test results (indicating microbiological activity), and the higher effects were detected for T8 lambs. The BP in lamb's diet increased the ruminal concentration of propionate (T4 and T8). The T8 lambs had greater serum activity of superoxide dismutase and glutathione transferase, and lower reactive oxygen species levels. We conclude that BP is a biotechnological additive with high nutritional potential.

Fumonisin-(Fusarium verticillioides)-contaminated feed causes hepatic oxidative stress and negatively affects broiler performance in the early stage: Does supplementation with açai flour residues (Euterpe oleracea) minimize these problems?

Fusarium verticillioides is often responsible for contamination of poultry feed with the mycotoxin fumonisin. The aim of this study was to determine whether oxidative stress caused by intake of fumonisin-contaminated feed affects broiler performance at an early stage of development, as well as to test whether the addition of açai residue flour to contaminated feed would minimize these negative effects of redox metabolism. Birds were divided into four groups, with four repetitions of five animals each: control (TC) - birds that received basal feed; TCA treatment - basal feed supplemented with 2% açai flour; TF treatment - feed experimentally contaminated with fumonisin (10 ppm); TFA treatment - fumonisin-contaminated feed (10 ppm) and supplemented with açai fluor (2%). The experiment lasted 20 days, that is, the first 20 days of the chicks' lives. At the end of the experiment, the birds were weighed, and blood, intestine and liver samples were collected. The TCA and TFA had greater body weights and weight gain than did TF. Further, TCA and TFA had lower feed conversion than did TF. Açai flour intake (TCA and TFA) stimulated albumin synthesis and reduced serum AST activity. Nitrate/nitrite (NOx) levels were higher in serum of fumonisin-challenged (TF) birds than in groups; NOx levels were also higher in the livers of all test groups (TF, TCA and TFA) than in TC. Serum glutathione S-transferase (GST) activity was lower in fumonisin-consuming groups (TF and TFA); this was different from what occurred in the liver, that is, higher GST activity in TF and lower activity in TFA than in TC. Catalase activity (CAT) was also higher in the fumonisin-challenged groups (TF and TFA) and the groups supplemented with açai flour (TCA) than in TC. Serum reactive species (RS) and TBARS (lipid peroxidation) levels in the liver were lower in birds supplemented with açai flour and exposed to fumonisin. These data suggest that the addition of açai flour in the feed of early chickens improves animal performance and minimizes the effects of hepatic oxidative stress in birds fed fumonisin-contaminated feed.

Mineral supplementation stimulates the immune system and antioxidant responses of dairy cows and reduces somatic cell counts in milk.

The aim of this study was to evaluate whether the use of subcutaneous mineral supplementation would affect metabolic parameters, immunological response, milk quality and composition of dairy cows in the postpartum period. Twelve pregnant primiparous Holstein cows, were divided into two groups: six animals supplemented with the mineral complex (magnesium, phosphorus, potassium, selenium and copper), and six animals used as controls. Milk samples were collected every two other weeks postpartum up to sixty days of lactation to analyze composition and quality. Blood samples were collected, and the levels of ketone bodies, total proteins, glucose, albumin, and globulin were measured. The catalase and superoxide enzymes, reactive oxygen species, tumor necrosis factor, and interleukins were determined. Animals supplemented with minerals showed lower levels of ketone bodies and somatic cell counts on days 30, 45 and 60 of the experiment, without changes in milk composition compared to the control group. Supplemented cows had lower levels reactive oxygen species and increased superoxide enzymes activity. Total protein, globulin and cytokine levels were higher in cows supplemented with mineral complexes. Therefore, we can conclude that subcutaneous mineral supplementation improved the immune response and minimized the oxidative stress in dairy cows during lactation.

Mineralization in newborn calves contributes to health, improve the antioxidant system and reduces bacterial infections.

The first phase of life of dairy calves has elevated mortality indices linked with low immunity and sanitary challenges, mainly bacterial infections are involved in the pathogenesis of diarrhea, the leading cause of death. Also, other important problem is the nutritional deficiencies, such as the mineral deficiency. Thus, the aim of this study was to evaluate whether an intramuscular mineral supplementation based on selenium, copper, potassium, magnesium and phosphorus possess beneficial effects on health of dairy calves. For this, ten calves were divided in two groups: the group A was supplemented with injectable mineral, while the group B was used as control group (without mineral supplementation). The mineral complex was administrated via intramuscularly at dose of 3 mL/animal on days 2 and 14 post-birth. The total blood was collected on days 2, 10, 20 and 30 of life of animals in order to analyze the antioxidant enzymes (catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx)), blood count and seric biochemistry linked with proteic, lipid and carbohydrate metabolism. Feces samples were also collected on days 10, 20 and 30 of life of animals to perform the total bacterial count, parasitological exam and fecal consistency score. Moreover, the weight and corporal temperature were also evaluated. The mineral supplementation presented beneficial properties to calves from birth to the 30th of life through the increase on activity of antioxidant enzymes, improvement of immunity, and avoiding problems linked with diarrhea and anemia, can be considered an interesting approach to prevent these alterations linked with high mortality in the period of life.

Curcumin attenuates memory deficits and the impairment of cholinergic and purinergic signaling in rats chronically exposed to cadmium.

This study investigated the protective effect of curcumin on memory loss and on the alteration of acetylcholinesterase and ectonucleotidases activities in rats exposed chronically to cadmium (Cd). Rats received Cd (1 mg/kg) and curcumin (30, 60, or 90 mg/kg) by oral gavage 5 days a week for 3 months. The animals were divided into eight groups: vehicle (saline/oil), saline/curcumin 30 mg/kg, saline/curcumin 60 mg/kg, saline/curcumin 90 mg/kg, Cd/oil, Cd/curcumin 30 mg/kg, Cd/curcumin 60 mg/kg, and Cd/curcumin 90 mg/kg. Curcumin prevented the decrease in the step-down latency induced by Cd. In cerebral cortex synaptosomes, Cd-exposed rats showed an increase in acetylcholinesterase and NTPDase (ATP and ADP as substrates) activities and a decrease in the 5'-nucleotidase activity. Curcumin was not able to prevent the effect of Cd on acetylcholinesterase activity, but it prevented the effects caused by Cd on NTPDase (ATP and ADP as substrate) and 5'-nucleotidase activities. Increased acetylcholinesterase activity was observed in different brain structures, whole blood and lymphocytes of the Cd-treated group. In addition, Cd increased lipid peroxidation in different brain structures. Higher doses of curcumin were more effective in preventing these effects. These findings show that curcumin prevented the Cd-mediated memory impairment, demonstrating that this compound has a neuroprotective role and is capable of modulating acetylcholinesterase, NTPDase, and 5'-nucleotidase activities. Finally, it highlights the possibility of using curcumin as an adjuvant against toxicological conditions involving Cd exposure. © 2015 Wiley Periodicals, Inc. Environ Toxicol 32: 70-83, 2017.

Supplementation with copper edetate in control of Haemonchus contortus of sheep, and its effect on cholinesterase's and superoxide dismutase activities.

The aim of this study was to evaluate the effect of copper edetate on biochemical parameters, oxidative profile, cholinesterase's activities, as well as its capacity to control gastrointestinal parasites in infected sheep. Thus, Lacaune sheep (n = 18) infected by Haemonchus contortus were used and divided into three groups of six animal each: the group A was composed of untreated animals (the control group), the group B was formed by animals treated with 0.3 mg/kg of copper edetate, and the group C was composed of animals treated with 0.5 mg/kg of copper edetate. Blood collection was performed on days 0, 10, 20 and 30 after mineral supplementation and different variables were measured. Cholinergic system was evaluated to determine the acetylcholinesterase (AChE) activity in total blood and butyrylcholinesterase (BChE) activity in serum. Eggs per gram of feces (EPG) were evaluated. There were no significant differences (P > 0.05) between groups regarding total protein, albumin, globulin and urea levels, GGT activity, as well as the hematocrit, and EPG. ALT activity decreased (P < 0.05) on groups B and C on day 30 compared to the control group (the group A). AChE activity decreased (P < 0.05) in the group C on days 10 and 30 compared to the control group, such decrease (P < 0.05) was also observed for BChE activity in the group C on day 10. ROS levels increased in the group C compared to groups A and B on day 10, while the SOD activity increased in the group C on days 20 and 30 compared to the control group (P < 0.05). CAT activity did not differ between groups (P > 0.05). In summary, the copper edetate was not efficient to control gastrointestinal parasites, but efficiently activated SOD, an important antioxidant enzyme. In addition, copper edetate was able to partially inhibit cholinesterase's activities when supplementated at its highest dose.

Diphenyl diselenide supplementation in infected mice by Toxoplasma gondii: Protective effect on behavior, neuromodulation and oxidative stress caused by disease.

The aim of this study was to evaluate the effect of subcutaneous administration of diphenyl diselenide (PhSe)2 on animal behavior and activities of acetylcholinesterase (AChE), adenylate kinase (AK), and creatine kinase (CK) in the brain of mice infected by Toxoplasma gondii. In addition, thiobarbituric acid reactive species (TBARS) levels and glutathione (GR, GPx and GST) activity were also evaluated. For the study, 40 female mice were divided into four groups of 10 animals each: group A (uninfected and untreated), group B (uninfected and treated with (PhSe)2), group C (infected and untreated) and group D (infected and treated with (PhSe)2). The mice were inoculated with 50 cysts of the ME49 strain of T. gondii. After infection the animals of the groups B and D were treated on days 1 and 20 post-infection (PI) with 5.0 µmol/kg of (PhSe)2 subcutaneously. Behavioral tests were conducted on days 29 PI to assess memory loss (object recognition), anxiety (elevated plus maze), locomotor and exploratory activity (Open Field) and it was found out that infected and untreated animals (group C) had developed anxiety and memory impairment, and the (PhSe)2 treatment did not reverse these behavioral changes on infected animals treated with (PhSe)2 (group D). The results showed an increase on AChE activity (P < 0.01) in the brain of infected and untreated animals (group C) compared to the uninfected and untreated animals (group A). The AK and CK activities decreased in infected and untreated animals (group C) compared to the uninfected and untreated animals (group A) (P < 0.01), however the (PhSe)2 treatment did not reverse these alterations. Infected and untreated animals (group C) showed increased TBARS levels and GR activity, and decreased GPx and GST activities when compared to uninfected and untreated animals (group A). Infected animals treated with (PhSe)2 (group D) decreased TBARS levels and GR activity, while increased GST activity when compared to infected and untreated animals (group C). It was concluded that (PhSe)2 showed antioxidant activity, but the dose used had no anti-inflammatory effect and failed to reverse the behavioral changes caused by the parasite.

Effect of zinc supplementation on ecto-adenosine deaminase activity in lambs infected by Haemonchus contortus: highlights on acute phase of disease.

Haemonchus contortus (order Strongylida) is a common parasitic nematode infecting small ruminants and causing significant economic losses worldwide. It induces innate and adaptive immune responses, which are essential for the clearance of this nematode from the host. Ecto-adenosine deaminase (E-ADA) is an enzyme that plays an important role in the immune system, while Zinc (Zn) has been found playing a critical role in E-ADA catalysis. Therefore, the aim of this study was to assess the effect of Zn supplementation on E-ADA activity in serum of lambs experimentally infected with H.contortus. To reach this purpose 28 male lambs (in average 25 kg) were used. The animals were divided into four groups: A and B composed of healthy animals (uninfected); C and D, infected with H.contortus. Groups B and D were supplemented with Zn Edetate, subcutaneously with 3 mg kg of live weight, on days 11 and 25 post-infection (PI). Blood and fecal samples were collected on the days 11, 25 and 39 PI, in order to assess hematocrit, seric E-ADA, and eggs per gram (EPG) counting, respectively. The animals of groups C and D showed severe hematocrit reduction (days 25 and 39 PI) and were EPG positive (days 11, 25 and 39 PI). On day 41 PI, three animals each group were subjected to necropsy. This procedure showed that animals of groups A and B did not have helminths in abomasum and intestines, while H.contortus were observed in groups C (5782.5 ± 810.9) and D (6185.0 ± 150.0). Infected and untreated animals (group C) showed a reduction in E-ADA activity, but this was not observed when the animals were supplemented with Zn (Group D). Therefore, based on our results, it was possible to observe that Zn supplementation exercised a positive effect on E-ADA activity in lambs infected with H.contortus, and did not allow a reduction in E-ADA activity, as occurred in the group infected and without supplementation. However, Zn supplementation was not able to prevent the worm burden.

Effects of iron supplementation on blood adenine deaminase activity and oxidative stress in Trypanosoma evansi infection of rats.

The aim of this study was to assess the effects of iron supplementation on oxidative stress and on the activity of the adenosine deaminase (ADA) in rats experimentally infected by Trypanosoma evansi. For this purpose, 20 rats were divided into four experimental groups with five animals each as follows: groups A and B were composed by healthy animals, while animals from groups C and D were infected by T. evansi. Additionally, groups B and D received two subcutaneous doses of iron (60 mg kg(-1)) within an interval of 5 days. Blood samples were drawn on day 8 post infection in order to assess hematological and biochemical variables. Among the main results are: (1) animals from group C showed reduced erythrogram (with tendency to anemia); however the same results were not observed for group D; this might be a direct effect of free iron on trypanosomes which helped to reduce the parasitemia and the damage to erythrocytes caused by the infection; (2) iron supplementation was able to reduce NOx levels by inhibiting iNOS, and thus, providing an antioxidant action and, indirectly, reducing the ALT levels in groups Band D; (3) increase FRAP levels in group D; (4) reduce ADA activity in serum and erythrocytes in group C; however, this supplementation (5) increased the protein oxidation in groups B and D, as well as group C (positive control). Therefore, iron showed antioxidant and oxidant effects on animals that received supplementation; and it maintained the activity of E-ADA stable in infected/supplemented animals.

Effect of zinc supplementation on E-ADA activity, seric zinc, and cytokines levels of Trypanosoma evansi infected Wistar rats.

The aim of this study was to evaluate the effect of zinc supplementation on the ecto-adenosine deaminase activity (E-ADA), zinc seric levels and cytokines (TNF-α, IL-1, IL-6, and IL -10) on rats experimentally infected by Trypanosoma evansi. Four groups with 10 rats each were used as negative controls (groups A and B), while the animals from the groups C and D were infected intraperitoneally with 0.1 mL of cryopreserved blood containing 1.4 × 10(4) of trypanosomes. Animals of groups B and D received two doses of Zinc (Zn) at 5 mg kg(-1), subcutaneously, on the 2nd and 7th day post-infection (PI). Blood samples were collected on days 5 (n = 5) and 15 PI (n = 5). Zn supplementation was able to increase the rat's longevity and to reduce their parasitemia. It was observed that seric Zn levels were increased on infected animals under Zn supplementation. Animals that were infected and supplemented with Zn showed changes in E-ADA activity and in cytokine levels (P < 0.05). Zn supplementation of healthy animals (Group B), increased the E-ADA activity, as well as reduced the concentration of cytokines. Infected animals from groups C and D showed increased levels of cytokines. Finally, we observed that Zn supplementation led to a modulation on cytokine's level in rats infected by T. evansi, as well as in E-ADA activity.

N-acetylcysteine prevents spatial memory impairment induced by chronic early postnatal glutaric acid and lipopolysaccharide in rat pups.

BACKGROUND AND AIMS: Glutaric aciduria type I (GA-I) is characterized by accumulation of glutaric acid (GA) and neurological symptoms, such as cognitive impairment. Although this disease is related to oxidative stress and inflammation, it is not known whether these processes facilitate the memory impairment. Our objective was to investigate the performance of rat pups chronically injected with GA and lipopolysaccharide (LPS) in spatial memory test, antioxidant defenses, cytokines levels, Na+, K+-ATPase activity, and hippocampal volume. We also evaluated the effect of N-acetylcysteine (NAC) on theses markers. METHODS: Rat pups were injected with GA (5 umol g of body weight-1, subcutaneously; twice per day; from 5th to 28th day of life), and were supplemented with NAC (150 mg/kg/day; intragastric gavage; for the same period). LPS (2 mg/kg; E.coli 055 B5) or vehicle (saline 0.9%) was injected intraperitoneally, once per day, from 25th to 28th day of life. Oxidative stress and inflammatory biomarkers as well as hippocampal volume were assessed. RESULTS: GA caused spatial learning deficit in the Barnes maze and LPS potentiated this effect. GA and LPS increased TNF-α and IL-1ß levels. The co-administration of these compounds potentiated the increase of IL-1ß levels but not TNF-α levels in the hippocampus. GA and LPS increased TBARS (thiobarbituric acid-reactive substance) content, reduced antioxidant defenses and inhibited Na+, K+-ATPase activity. GA and LPS co-administration did not have additive effect on oxidative stress markers and Na+, K+ pump. The hippocampal volume did not change after GA or LPS administration. NAC protected against impairment of spatial learning and increase of cytokines levels. NAC Also protected against inhibition of Na+,K+-ATPase activity and oxidative markers. CONCLUSIONS: These results suggest that inflammatory and oxidative markers may underlie at least in part of the neuropathology of GA-I in this model. Thus, NAC could represent a possible adjuvant therapy in treatment of children with GA-I.

Pre-treatment with curcumin modulates acetylcholinesterase activity and proinflammatory cytokines in rats infected with Trypanosoma evansi.

The potent activity against Trypanosomes and health beneficial effects of curcumin (Cur) has been demonstrated in various experimental models. In this study, we evaluated the in vivo effect of Cur as trypanocide and as potential anti-inflammatory agent, through the evaluation of immunomodulatory mechanisms in rats infected with Trypanosoma evansi. Daily oral Cur was administered at doses of 0, 20 or 60mg/kg as preventive treatment (30 and 15days pre infection) and as treatment (post infection). The treatment of the groups continued until the day of euthanasia. Fifteen days after inoculation, parasitemia, plasma proinflammatory cytokines (IFN-γ, TNF-α, IL-1, IL-6), anti-inflammatory cytokines (IL-10) and blood acetylcholinesterase activity (AChE) were analyzed. Pretreatment with Cur reduced parasitemia and lethality. Cur inhibited AChE activity and improved immunological response by cytokines proinflammatory, fundamental during T. evansi infection. We found that Cur is not so important as an antitrypanosomal activity but as immunomodulator agent. These findings reveal that the preventive use of Cur stimulates anti-inflammatory mechanisms, reducing an excessive inflammatory response.

NTPDase and 5'-nucleotidase activities from synaptosomes and platelets of rats exposed to cadmium and treated with N-acetylcysteine.

The purpose of the present investigation was to evaluate the hydrolysis of adenine nucleotides on synaptosomes and platelets obtained from rats exposed to cadmium (Cd) and treated with N-acetylcysteine (NAC). Rats received Cd (2 mg/kg) and NAC (150 mg/kg) by gavage every other day for 30 days. Animals were divided into four groups (n = 4-6): control/saline, NAC, Cd, and Cd/NAC. The results of this study demonstrated that NTPDase and 5'-nucleotidase activities were increased in the cerebral cortex synaptosomes of Cd-poisoned rats, and NAC co-treatment reversed these activities to the control levels. In relation to hippocampus synaptosomes, no differences on the NTPDase and 5'-nucleotidase activities of Cd-poisoned rats were observed and only the 5'-nucleotidase activity was increased by the administration of NAC per se. In platelets, Cd-intoxicated rats showed a decreased NTPDase activity and no difference in the 5'-nucleotidase activity; NAC co-treatment was inefficient in counteracting this undesirable effect. Our findings reveal that adenine nucleotide hydrolysis in synaptosomes and platelets of rats were altered after Cd exposure leading to a compensatory response in the central nervous system and acting as a modulator of the platelet activity. NAC was able to modulate the purinergic system which is interesting since the regulation of these enzymes could have potential therapeutic importance. Thus, our results reinforce the importance of the study of the ecto-nucleotidases pathway in poisoning conditions and highlight the possibility of using antioxidants such as NAC as adjuvant against toxicological conditions.

Hematological indices and activity of NTPDase and cholinesterase enzymes in rats exposed to cadmium and treated with N-acetylcysteine.

The present study aimed to investigate the influence of N-acetylcysteine (NAC) on cadmium (Cd) poisoning by evaluating Cd concentration in tissues, hematological indices as well as the activity of NTPDase, acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) enzymes of rats exposed to Cd and co-treated with NAC. For this purpose, the rats received Cd (2 mg/kg) and NAC (150 mg/kg) by gavage every other day for 30 days. Animals were divided into four groups (n = 6-8): control/saline, NAC, Cd, and Cd/NAC. Cd exposure increased Cd concentration in plasma, spleen and thymus, and NAC co-treatment modulated this augment in both lymphoid organs. Cd exposure reduced red blood cell count, hemoglobin content and hematocrit value. Cd intoxication caused a decrease in total white blood cell count. NAC treatment per se caused an increase in lymphocyte and a decrease in neutrophil counts. On contrary, Cd exposure caused a decrease in lymphocyte and an increase in neutrophil and monocyte counts. NAC reversed or ameliorated the hematological impairments caused by Cd poisoning. There were no significant alterations in the NTPDase activity in lymphocytes of rats treated with Cd and/or NAC. Cd caused a decrease in the activities of lymphocyte AChE, whole blood AChE and serum BChE. However, NAC co-treatment was inefficient in counteracting the negative effect of Cd in the cholinesterase activities. The present investigation provides ex vivo evidence supporting the hypothesis that Cd induces immunotoxicity by interacting with the lymphoid organs, altering hematological parameters and inhibiting peripheral cholinesterase activity. Also, it highlights the possibility to use NAC as adjuvant against toxicological conditions.

Behavior and brain enzymatic changes after long-term intoxication with cadmium salt or contaminated potatoes.

This study investigated the cadmium (Cd) intoxication on cognitive, motor and anxiety performance of rats subjected to long-term exposure to diet with Cd salt or with Cd from contaminated potato tubers. Potato plantlets were micropropagated in MS medium and transplanted to plastic trays containing sand. Tubers were collected, planted in sand boxes and cultivated with 0 or 10 µM Cd and, after were oven-dried, powder processed and used for diet. Rats were divided into six groups and fed different diets for 5 months: control, potato, potato+Cd, 1, 5 or 25 mg/kg CdCl2. Cd exposure increased Cd concentration in brain regions. There was a significant decrease in the step-down latency in Cd-intoxicated rats and, elevated plus maze task revealed an anxiolytic effect in rats fed potato diet per se, and an anxiogenic effect in rats fed 25 mg/kg Cd. The brain structures of rats exposed to Cd salt or Cd from tubers showed an increased AChE activity, but Na+,K+-ATPase decreased in cortex, hypothalamus, and cerebellum. Therefore, we suggest an association between the long-term diet of potato tuber and a clear anxiolytic effect. Moreover, we observed an impaired cognition and enhanced anxiety-like behavior displayed by Cd-intoxicated rats coupled with a marked increase of brain Cd concentration, and increase and decrease of AChE and Na+,K+-ATPase activities, respectively.