Effect of Selenium Pre-treatment on Antioxidative Enzymes and Lipid Peroxidation in Cd-exposed Suckling Rats

Since there are no data about the protective role of selenium (Se) against cadmium (Cd)-induced oxidative damage in early life, we studied the effect of Se supplementation on antioxidative enzyme activity and lipid peroxidation (through thiobarbituric acid reactive substances; TBARS) in suckling Wistar rats exposed to Cd. Treated animals received either Se alone for 9 days (8 μmol, i.e., 0.6 mg Se as Na₂SeO₃ kg⁻¹ b.w., daily, orally; Se group), Cd alone for 5 days (8 μmol, i.e., 0.9 mg Cd as CdCl₂ kg⁻¹ b.w., daily, orally; Cd group), or pre-treatment with Se for 4 days and then co-treatment with Cd for the following 5 days (Se + Cd group). Our results showed that selenium supplementation, with and without Cd, increased SOD activity in the brain and kidney, but not in the liver and GSH-Px activity across all tissues compared to control rats receiving distilled water. Relative to the Cd group, Se + Cd group had higher kidney and brain SOD and GSH-Px activity (but not the liver), while in the liver caused increased and in the brain decreased TBARS level. These results suggest that Se stimulates antioxidative enzymes in immature kidney and brain of Cd-exposed rats and could protect against oxidative damage.     

Zinc or Magnesium Supplementation Modulates Cd Intoxication in Blood,Kidney, Spleen,and Bone of Rabbits

The objective of this study was to examine the influence of oral supplementation with Zn or Mg on Cd content in the blood and organs of rabbits exposed to prolonged Cd intoxication. Rabbits were divided into the following groups: Cd group-received orally every day for 4 weeks 10 mg Cd/kg body weight (b.w.), Cd+Zn group and Cd+Mg group-exposed to Cd and supplemented with 20 mg Zn/kg b.w. or 40 mg Mg/kg b.w. 1 h after Cd treatment. Cd content in biological material was determined by atomic absorption spectrophotometry. Blood Cd concentration was determined in all investigated groups at time 0 and after 10, 14, 18, 22, 25, and 28 days, whereas Cd content in the brain, heart, lungs, liver, kidney, spleen, pancreas, skeletal muscle, and bone was determined after 28 days. Blood Cd concentration was significantly increased in all groups from the 14th day of Cd intoxication and lasted till the end of the experiment. Zn or Mg supplementation significantly reduced blood Cd content on the 18th and 25th days. Supplementation with Zn or Mg significantly decreased Cd concentration in the kidney, spleen, and bone and, in addition, Zn reduced Cd content in the brain. Supplementation with Zn or Mg in Cd-intoxicated rabbits caused similar reduction of blood Cd concentration; however, reduction of tissue Cd content was more pronounced in Zn- than in Mg-supplemented group.     

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.     

Effects of zinc pre-treatment on blood glutathione,serum zinc and kidney histological organisation in male rats exposed to cadmium

The effects of sub-chronic exposure to cadmium (Cd) on the blood glutathione, serum zinc and on the kidney histological organisation in rats as well as the possible protective role of zinc (Zn) are the object of this study. For this purpose, 60 male Wistar rats (8 weeks old) were divided into three groups: the first group was exposed to Cd in the form of CdCl₂, administered in five doses (each of 0.4 mg Cd/kg b.w.) on days 5, 10, 15, 20 and 25, giving a total dose of 2 mg Cd/kg b.w., i.p.; the second group was simultaneously exposed to Zn and Cd with the same timeline and the same doses of Cd as the first group but with, in addition, injections of Zn in the form of ZnCl₂, administered in doses of 0.8 mg Zn/kg b.w., giving a total dose of 4 mg Zn/kg b w, i.p.; a control group received 0.5 mL of physiological saline in an identical manner. Intoxication with Cd was followed by a significant decrease in blood glutathione, increase in oxidized glutathione as well as histological damage in kidneys. Pre-treatment with Zn exhibited a protective role against Cd toxicity with a significant decrease in serum zinc content. This fact may be explained by an excessive use of zinc in metallothionein synthesis as a cadmium detoxification agent.     

Histopathology and cytotoxicity as biomarkers in treated rats with cadmium and some therapeutic agents

The present study aimed to investigate the protective role of ascorbic acid (vitamin C) and zinc (Zn) against cadmium (Cd) induced histopathological changes in tissues of liver, kidney, lung and testis of rats as well as chromosomal aberrations. For this purpose, 60 male albino rats were divided into six groups; each group contained 10 animals. The first group served as control and was given only distilled water. The second and third groups received distilled water supplemented with 2 g ascorbic acid/l and 500 mg Zn/l, respectively. The fourth group received a daily oral dose containing 3 mg Cd/kg b.w. (1/30 LD₅₀). The fifth group received Cd + ascorbic acid (3 mg Cd/kg b.w. + 2 g ascorbic acid/l), while the sixth group received Cd + Zn (3 mg Cd/kg b.w. +500 mg Zn/l). The treatment in all groups lasted for 90 consecutive days. Rats exposed to cadmium showed severe histopathological changes in the liver, kidney, lung and testicular tissues as well as chromosomal aberrations such as: break, ring, centromeric separation and polyploidy. Co-treatment with zinc partially improved the histopathological changes and chromosomal aberrations while co-treatment with vitamin C exhibited a more protective role and markedly reduced tissues damage induced by Cd.     

Doxorubicin-induced alterations in kidney functioning,oxidative stress,DNA damage,and renal tissue morphology; Improvement by Acacia hydaspica tannin-rich ethyl acetate fraction

Doxorubicin (DOX) is an anthracycline drug used for cancer treatment. However, its treatment is contiguous with toxic effects. We examined the nephroprotective potential of A. hydaspica polyphenol-rich ethyl acetate extract (AHE) against DOX persuaded nephrotoxicity. 36 male Sprague Dawley rats were randomly assorted into 6 groups. Control group received saline; DOX group: 3 mg/kg b.w. dosage of DOX intraperitoneally for 6 weeks (single dose/week). In co-treatment groups, 200 and 400 mg/kg b.w AHE was given orally for 6 weeks in concomitant with DOX (3 mg/kg b.w, i.p. injection per week) respectively. Standard group received silymarin 400 mg/kg b.w daily + DOX (single dose/week). Biochemical kidney function tests, oxidative stress markers, genotoxicity, antioxidant enzyme status, and histopathological changes were examined. DOX caused significant body weight loss and decrease kidney weight. DOX-induced marked deterioration in renal function indicators in both urine and serum, i.e., PH, specific gravity, total protein, albumin, urea, creatinine, uric acid, globulin, blood urea nitrogen, etc. Also, DOX treatment increases renal tissue oxidative stress markers, while lower antioxidant enzymes in tissue along with degenerative alterations in the renal tissue compared to control rats. AHE co-treatment ameliorates DOX-prompted changes in serum and urine chemistry. Likewise, AHE treatment decreases sensitive markers of oxidative stress and prevented DNA damages by enhancing antioxidant enzyme levels. DOX induction in rats also caused DNA fragmentation which was restored by AHE co-treatment. Moreover, the histological observations evidenced that AHE effectively rescued the kidney tissue from DOX interceded oxidative damage. Our results suggest that co-treatment of AHE markedly improve DOX-induced deleterious effects in a dose-dependent manner. The potency of AHE co-treatment at 400 mg/kg dose is similar to silymarin. These outcomes revealed that A. hydaspica AHE extract might serve as a potential adjuvant that avoids DOX-induced nephrotoxicity.     

Dietary Magnesium Sulfate Supplementation Protects Heat Stress-Induced Oxidative Damage by Restoring the Activities of Anti-oxidative Enzymes in Broilers

The purpose of this study was to investigate the effect of dietary magnesium sulfate supplementation on heat stress-induced oxidative damage in broilers. One hundred twenty 14-day-old broilers were randomly assigned into four treatment groups with three replicates of ten birds each. The broilers were reared under normal ambient temperature (24 ± 1°C) fed with a basal (control) diet or reared under high ambient temperature (35 ± 1°C between 1000 and 1800 h, 8 h each day) fed with a basal diet supplemented with magnesium sulfate (0, 2.5 or 5.0 mg/kg of diet) from 14 to 42 days of age. Growth performance and oxidative damage were evaluated in each treatment group. Our results demonstrated that dietary magnesium sulfate supplementation significantly prevented heat stress-induced oxidative damage and improved growth performance in broilers compared with that of control. Mechanistically, this beneficial effect was mediated, at least partly, by restoring the activity of anti-oxidative enzymes. This finding suggests that magnesium sulfate supplementation might be a potential strategy to attenuate heat stress-induced detrimental effects in broilers raised in summer season or tropical areas.     

Hepatoprotective and antioxidant activity of N-Trisaccharide in different experimental rats

ObjectivesTo investigate the hepatoprotective, antioxidant and antihyperlipidemic effect of N-Trisaccharide isolated from Cucumis prophetarum (L.) on different experimental rats.MethodsN-Trisaccharide (25 and 50 mg/kg.b.w), silymarin (25 mg/kg) and glibenclamide (25 mg/kg) was orally administered once daily for 28 days and toxicity evaluation studies were carried out. Liver damage was assessed by determining DNA damage, serum enzyme activities and hepatic histopathology of carbon tetrachloride (CCl₄) induced hepatic injury in rats. Enzymatic and non enzymatic antioxidant levels in liver and kidney were determined and biochemical parameters such as, serum lipid profile, renal function markers were estimated in type 2 diabetic rats.ResultsDNA fragmentation analysis revealed the protective effect of N-Trisaccharide on liver DNA damage. Histopathological studies indicated that CCl₄-induced liver injury was less severe in N-Trisaccharide (25 and 50 mg/kg) treated group. Given at the above doses conferred significant protection against the hepatotoxic actions of CCl₄ in rats, reducing serum markers like SGOT, SGPT, ALP, creatinine and urea levels back to near normal (p < 0.05) compared to untreated rats. In diabetic rats, N-Trisaccharide treatment significantly reversed abnormal status of enzymatic and non-enzymatic antioxidants levels to near normal. Also, serum lipids such as TG, TC, LDL-C and VLDL-C levels were significantly (p < 0.05) reduced compared to diabetic untreated rats.ConclusionPresent study results confirm that N-Trisaccharide possesses significant antihyperlipidemic, antioxidant and hepatoprotective properties.     

Liver and kidney concentrations of selenium in wild boars (<Emphasis Type="Italic">Sus scrofa</Emphasis>) from northwestern Poland

The aim of this study was to determine liver and kidney concentrations of selenium in wild boars from the northwest part of Poland, depending on season of the year, age, sex, and body weight. Altogether, samples of livers and kidneys from 172 wild boars that were shot in 2005–2008 were investigated. Liver and kidney concentrations of selenium were determined using spectrofluorometric method. In all the animals studied, selenium concentration was several times lower in the liver than in the kidneys. Selenium concentration averaged 0.19 μg/g wet weight (w.w.) in the liver and 1.20 μg/g w.w. in kidneys. The present study showed that season (P ≤ 0.05), age (P ≤ 0.01), and body weight (P ≤ 0.01) have a significant effect on selenium concentration in the liver of wild boars. Liver selenium concentration was the highest in spring (0.23 μg/g w.w.) and the lowest in autumn (0.16 μg/g w.w). Young animals (up to 1 year of age) and those with the lowest body weight (up to 20 kg) were characterized by a slightly lower selenium concentration in the liver compared to older and heavier animals. No significant differences were found in organ selenium concentration between males and females. According to biochemical criteria for the diagnosis of selenium deficiency in pig liver, which were used to evaluate selenium concentration in the liver of wild boars, no individuals were found to have optimal levels. Considering that in Se deficiency higher selenium concentrations are found in kidneys than in the liver, it can be presumed that the wild boars had Se deficiency. However, this is difficult to state conclusively because there are no reference values for this species.     

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.     

Influence of Dietary Copper Methionine Concentrations on Growth Performance,Digestibility of Nutrients,Serum Lipid Profiles,and Immune Defenses in Broilers

A 42-day experiment was conducted to evaluate the influence of dietary copper (Cu) concentrations on growth performance, nutrient digestibility, and serum parameters in broilers aged from 1 to 42 days. Five hundred forty 1-day-old broilers were randomly assigned into 1 of the following 6 dietary treatments: (1) control (basal diet without supplemental Cu), (2) 15 mg/kg supplemental Cu (Cu15), (3) 30 mg/kg supplemental Cu (Cu30), (4) 60 mg/kg supplemental Cu (Cu60), (5) 120 mg/kg supplemental Cu (Cu120), and (6) 240 mg/kg supplemental Cu (Cu240), Cu as copper methionine. A 4-day metabolism trial was conducted during the last week of the experiment feeding. The results showed that dietary Cu supplementation increased the average daily gain and the average daily feed intake (P < 0.01). The feed gain ratio, however, was not affected by dietary Cu (P > 0.10). Additionally, dietary Cu supplementation increased the digestibility of fat and energy (P < 0.05). The concentration of serum cholesterol, triglycerides, and high-density lipoprotein cholesterol decreased with dietary Cu supplementation (P < 0.05). The activities of serum Cu-Zn superoxide dismutase (P < 0.05), glutathione peroxidase (P < 0.05), and ceruloplasmin (P = 0.09), on the contrary, were increased by Cu addition. For immune indexes, dietary Cu supplementation increased serum IgA and IgM (P < 0.05). In addition, the activities of serum ALT increased with increasing dietary Cu supplementation (P < 0.05). In conclusion, our data suggest that Cu supplementation can increase fat digestibility and promote growth. Additionally, dietary Cu supplementation can reduce serum cholesterol and enhance antioxidant capacity in broilers.

     

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.     

Restorative effects of Chrysin pretreatment on oxidant–antioxidant status,inflammatory cytokine production,and apoptotic and autophagic markers in acute paracetamol‐induced hepatotoxicity in rats: An experimental and biochemical study

Paracetamol (PC) is a widely used analgesic and antipyretic drug, but it leads to acute hepatotoxicity at high doses intakes. This study was aimed to investigate the effects of Chrysin (CR) on hepatotoxicity constituted at high doses of PC in rats. Rats were subjected to oral pretreatment of CR (25 and 50 mg/kg b.w.) via feeding needle for 6 days against hepatotoxicity induced by a single dose of PC (500 mg/kg b.w.) administered orally via feeding needles. Although PC increases lipid peroxidation and liver enzyme activities, it has led to reduction of antioxidant enzyme activities. PC induced inflammatory responses by increasing the levels of TNF‐α and IL‐1β. Furthermore, PC caused apoptosis and autophagy by increasing activity of Caspase‐3 and LC3B level. On the other hand, CR therapy significantly regulated these values in rats. This study demonstrated that CR possesses restorative effect against PC‐induced hepatotoxicity by suppressing oxidative stress, inflammation, and apoptotic and autophagic tissue damage.     

Investigation of in vitro and in vivo antioxidant potential of secoisolariciresinol diglucoside

The present study was designed to evaluate the in vitro and in vivo ameliorative antioxidant potential of secoisolariciresinol diglucoside (SDG). In vitro antioxidant activity of synthetic SDG was carried out using DPPH, reducing power potency, and DNA protection assays. Wistar albino rats weighing 180–220 g were used for in vivo studies and liver damage was induced in the experimental animals by a single intraperitoneal (I.P.) injection of CCl₄ (2 g/kg b.w.). Intoxicated animals were treated orally with synthetic SDG at (12.5 and 25 mg/kg b.w.) and Silymarin (25 mg/kg) for 14 consecutive days. The levels of catalase (CAT), superoxide dismutase (SOD), peroxidase (POX), and lipid peroxidase (LPO) were measured in liver and kidney homogenates. The synthetic SDG exerts high in vitro antioxidant potency as it could scavenge DPPH at a IC₅₀ value of 78.9 μg/ml and has dose-dependent reducing power potency and protected DNA at 0.5 mg/ml concentration. Oral administration of synthetic SDG at 12.5 and 25 mg/kg b.w. showed significant protection compared to Silymarin (25 mg/kg) and the activities of CAT, SOD, and POX were markedly increased (P < 0.05), whereas LPO significantly decreased (P < 0.001) in a dose-dependent manner in liver and kidney in both pre- and post-treatment groups when compared to toxin-treated group. The results of in vitro and in vivo investigations revealed that synthetic SDG at 25 mg/kg b.w. is associated with beneficial changes in hepatic enzyme activities and thereby plays a key role in the prevention of oxidative damage in immunologic system.     

Beneficial role of naringin, a flavanoid on nickel induced nephrotoxicity in rats

This study was conducted to investigate the beneficial role of naringin on nickel induced nephrotoxicity. Nickel (Ni) (20 mg/kg body weight (b.w.) was administered intraperitoneally (i.p.) for 20 days. Naringin was administered orally (20, 40 and 80 mg/kg b.w.) with i.p. administration of Ni. Ni administration increased the levels of serum urea, uric acid and creatinine with a significant decrease in creatinine clearance and decreased levels of urea, uric acid and creatinine in urine. The levels of lipid peroxidation markers and nickel concentration in blood and kidney were also increased. While, the activities of enzymic and non-enzymic antioxidants were decreased. Treatment with naringin attenuated the alterations in the renal and urine markers, decreasing lipid peroxidation markers, increasing the antioxidant cascade and decreasing the nickel concentration in blood and kidney. All these changes were supported by histopathological observations. These findings demonstrate that naringin exerts a protective effect against nickel toxicity.     

Role of oregano on bacterial enzymes in 1,2-dimethylhydrazine-induced experimental colon carcinogenesis

Colon cancer incidence is higher in developed countries than in developing countries. We determined the effect of oregano (Origanum vulgare L.) on fecal bacterial enzyme activities in 1,2-dimethylhydrazine (DMH)-induced experimental colon carcinogenesis in rats. Male Wistar albino rats were divided into 6 groups and all animals were fed with a high-fat diet (20% fat in the diet). Group 1 served as control and group 2 animals received 60 mg.kg(-1) body weight (b.w.) oregano daily for 15 weeks. To induce colon cancer, DMH (20 mg.kg(-1) b.w.) was injected subcutaneously once a week for the first 4 weeks (groups 3-6). In addition, oregano was administered at 20, 40, or 60 mg.kg(-1) b.w. each day orally for the entire 15 weeks (groups 4-6). We analyzed the fecal bacterial enzyme activities and found it to be significantly higher in the group treated with DMH alone than in the control group. Oregano supplementation at all 3 doses significantly suppressed the bacterial enzyme activities and modulated oxidative stress significantly compared with the unsupplemented DMH-treated group. Results of our present investigation therefore revealed that oregano markedly inhibited DMH-induced colon carcinogenesis and that the optimal dose of 40 mg.kg(-1) b.w. was more effective than either the higher or lower doses.     

Molecular and biochemical investigations on the effect of quercetin on oxidative stress induced by cisplatin in rat kidney

The present study was aimed to investigate the ability of quercetin (QE) to ameliorate adverse effects of cisplatin (Cis.) on the renal tissue antioxidants by investigating the kidney antioxidant gene expression and the antioxidant enzymes activity. Forty rats divided into. Control rats. QE treated rats were orally administered 100 mg QE/kg for successive 30 days. Cis. injected rats were administered i.p. Cis. (12 mg/kg b.w.) for 5 mutual days. Cis. + QE rats were administered Cis. i.p. (12 mg/kg) and orally administered 100 mg QE/kg for consecutive 30 days. The obtained results indicated that Cis. induced oxidative stress in the renal tissue. That was through induction of free radical production, inhibition of the activity of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione reductase (GR) as well their genes expression. At the same time, vitamin E, vitamin C and reduced glutathione (GSH) levels were decreased. QE had the ability to overcome cisplatin-induced oxidative stress through the reduction of free radical levels. The antioxidant genes expression and antioxidant enzymes activity were induced. Finally the vitamin E, vitamin C and GSH levels were increased. Our work, proved the renoprotective effects of QE against oxidative stress induced by cisplatin.     

Cadmium-induced oxidative stress and DNA damage in kidney of pregnant female rats

In the present study, we have investigated the influence of sub-acute treatment with cadmium (Cd) on some parameters indicative of oxidative stress and DNA damage in tissues of pregnant female rats. Pregnant female rats (n=6) were injected subcutaneously, daily with a dose of cadmium chloride of 3 mg/kg body weight (b.w.) from day 6 to day 19 of pregnancy, and they were allowed to deliver normally. MDA level and GPx, CAT and SOD activities were used as markers of oxidative stress in liver and kidney. The 8-oxo-dG level was measured by the HPLC-EC system. Cd treatment increased MDA (+116%, p<0.01) in kidney. Moreover, Cd treatment also decreased CuZn-SOD (-11%, p<0.05) and GSH level (-52%, p<0.05) in kidney. Treated rats displayed an increase of the liver metallothionein (MT) level. Induction of MT in liver was probably implicated in the detoxification of Cd. The high level of Cd (3 mg/kg) used in the present study is partially neutralized by MT in liver, whereas the free fraction could be implicated in the oxidative stress and DNA oxidation observed in kidney. Cd treatment failed to alter 8-oxodGuo, indicating the absence of DNA oxidation in liver; by contrast, the same treatment increased the 8-oxodGuo level (+51%, p<0.05) in the kidney of pregnant female rats, indicating an oxidative stress associated with DNA damage only in kidney.     

Effects of Dietary Supplementation of Recombinant Plectasin on Growth Performance,Intestinal Health and Innate Immunity Response in Broilers

The present study was conducted to evaluate the effects of dietary supplementation of recombinant plectasin (Ple) on the growth performance, intestinal health, and serum immune parameters in broilers. A total of 288 1-day-old male broilers (Arbor Acres) were randomly allotted to four dietary treatments including the basal diet (NC) and basal diet supplemented with 10 mg enramycin/kg (PC), 100 mg Ple/kg (LPle), and 200 mg Ple/kg (HPle) diets. The results indicated Ple increased (P < 0.01) average daily gain and decreased (P ≤ 0.02) feed to gain ratio of broilers. In addition, the supplementation of Ple in the diets increased (P ≤ 0.01) duodenal lipase (day 21) and trypsin (day 42) activities compared with the NC group. Similar as the supplementation of enramycin, Ple also increased villus height and decreased crypt depth in jejunum (day 21), and thus the villus height to crypt depth ratio (P < 0.01) was increased compared to the NC group on day 42. The serum immunoglobulin M (days 21 and 42), immunoglobulin G (day 42), complement 3 (day 21), and complement 4 (days 21 and 42) were significantly increased (P ≤ 0.02) due to the supplementation of Ple and enramycin, while the concentration of malondialdehyde in jejunum was decreased (P < 0.01) in PC, LPle, and HPle groups on day 21 compared with those in the NC group. Furthermore, Ple reduced (P < 0.01) Escherichia coli and total aerobic bacteria population in ileum and cecum of birds on days 21 and 42. These results indicate that the recombinant plectasin has beneficial effects on growth performance, intestinal health, and innate immunity in broilers.

     

The antidiabetic and anticholinergic effects of chrysin on cyclophosphamide‐induced multiple organ toxicity in rats: Pharmacological evaluation of some metabolic enzyme activities

Chrysin (CH) or 5,7‐dihydroxyflavone is a flavonoid present in various plants, bee propolis, and honey. Cyclophosphamide (CYP) is a chemotherapeutic drug, which is extensively used in the treatment of multiple human malignancies. In our study, we aimed to investigate the effects of CYP and CH on some metabolic enzymes including carbonic anhydrase, aldose reductase, paraoxonase‐1, α‐glycosidase, acetylcholinesterase, and butyrylcholinesterase enzyme activities in the brain, heart, testis, liver, and kidney tissues of rats. Thirty‐five adult male Wistar rats were used. The animals were pretreated with CH (25 and 50 mg/kg b.w.) for seven days before administering a single dose of CYP (200 mg/kg b.w.) on the seventh day. In all the tissues, the treatment of CH significantly regulated these enzyme activities in CYP‐induced rats. These results showed that CH exhibited an ameliorative effect against CYP‐induced brain, heart, liver, testis, and kidney toxicity.