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This study explored the combined influence of tank color, stocking density, and gender on Tilapia zillii's performance and well‐being. In this 120‐day trial, 320 T. zillii, each initially weighing 10.0 ± 0.1 g/fish, were distributed among 24 tanks. The experiment included eight distinct treatment combinations, varying tank color (blue and green), stocking density (10 and 30 fish/m3) and sex (monosexual and mixed). The results showed that blue tanks improved specific growth rate and condition factor, while green tanks were better for feed utilization. Density at 30 fish/m3 showed the highest mean values of final body weight and total length, weight gain (WG), and gain length. Mono‐sex outperformed mixed‐sex ones in WG and daily growth. Interactions between color, density and sex were significant, affecting growth and feed utilization. Green tanks were best for protein profiles, while blue tanks excelled in glucose. A density of 10 fish/m3 yielded the highest protein profiles, and mono‐sex fish had higher protein profiles. For lipid profiles, green tanks were superior, and density affected lipid profiles. Mixed‐sex populations were best for certain lipid profile parameters. Interactions between these factors also played a significant role, making the biochemical profiles of T. zillii a complex interplay of various factors. The results explored that tank color, fish density and sex influence the activity of nonspecific immune enzymes in the liver of T. zillii. Blue tanks and lower fish density led to higher nonspecific immune enzymes, while mono‐sex fish exhibited more significant nonspecific immune enzymes. Complex interactions between these factors also influenced nonspecific immune enzyme activities. Blue tanks increased malondialdehyde (MDA) levels, while green tanks raised glutathione S‐transferases (GST) and catalase (CAT) levels. Lower fish density led to higher MDA, while higher density increased GST and CAT. Mono‐sex fish had more MDA and GST, while mixed‐sex fish showed greater CAT levels. Complex interactions among these factors affected the antioxidant levels in T. zillii. In summary, our study suggests that rearing T. zillii in green tanks at higher densities (30 fish/m3) and in mono‐sex conditions yields the best results in terms of growth and overall performance. [ABSTRACT FROM AUTHOR]

This study was conducted to investigate the protective potential of a pharmaceutically formulated capsule of artichoke leaf powder (ArLP) against aflatoxin B1 (AFB1)-induced hepatotoxicity in male albino rats. In the 42-day experiment, rats were divided into five equal groups: (i) control, treated with sterile water, (ii) treated with 4% DMSO as AFB1 vehicle, (iii) ArLP of 100 mg kg–1 bw, (iv) AFB1 of 72 µg kg–1 bw, and (v) AFB1 plus ArLP. Exposure of rats to AFB1 resulted in hepatotoxicity as manifested by the intensification of oxidative stress, production of free radicals and significant increase in the activity levels of liver function enzymes relative to the control. Significant reductions in both the enzymatic and non-enzymatic antioxidant markers as well as histopathological abnormalities in liver tissues were also observed. Notably, the combined administration of ArLP with AFB1 clearly reduced AFB1-mediated adverse effects leading to the normalization of most of these parameters back to control levels. These findings clearly highlight the potential benefits of artichoke dietary supplements as a safe and natural solution in counteracting the adverse hepatotoxic effects conferred by AFB1 exposure. Further research is warranted to fully dissect the biochemical and molecular mechanism of action of the observed artichoke-mediated hepatoprotection. [ABSTRACT FROM AUTHOR]

Attenuation of adverse effects of aflatoxin (AFB1) in brains of B1 rats by extracts of leaves of artichoke was studied. The active ingredients in extracts of leaves of artichoke, Cynara scolymus L., were determined by HPLC analysis. In the 42-day experiment, rats were exposed to either sterile water, 4% DMSO, 100 mg artichoke leaf extract/kg body mass, 72 μg aflatoxin B1/kg body mass, or AFB1 plus artichoke leaf extract. Neurotoxicity of AFB1 was determined by an increase in profile of lipids, augmentation of plasmatic glucose and concentrations of insulin, oxidative stress, increased activities of cholinergic enzymes, and a decrease in activities of several antioxidant enzymes and pathological changes in brain tissue. Extracts of artichoke leaf significantly reduced adverse effects caused by AFB1, rescuing most of the parameters to values similar to unexposed controls, which demonstrated that adverse, neurotoxic effects caused by aflatoxin B1 could be significantly reduced by simultaneous dietary supplementation with artichoke leaf extract, which itself is not toxic. [ABSTRACT FROM AUTHOR]

Free radicals are involved in neurodegenerative disorders such as ischemia and aging. Treatments with Spirulina have been shown to reduce neurodegenerative changes in animals. The present study has been designed to examine the potential neuroprotective effects of Spirulina platensis (Sp.) against AlCl3-induced neurotoxicity in different regions of brain (cerebral cortex, hippocampus and hind brain) of rats. AlCl3 caused significant increase in thiobarbituric acid-reactive substances, tumor necrosis factor-α and aluminium concentration, while decrease glutathione, total antioxidant capacity, antioxidant enzymes (SOD, CAT, GST and GPx), total thiol content, monoamine oxidase, Na+-K+ ATPase and total ATPase. These results were confirmed by histopathological and fluorescence examination of different regions of brain. Cerebral cortex and hippocampus of AlCl3 showed loss of normal structure, neuronal degeneration and increase in the number of neurodegenerative features, more illuminated aggregates, higher fluorescence emission intensity in the presence of amyloid protein fibrils. While, the presence of Spirulina with AlCl3 in the combination group exhibited more normal neurons with few pyknotic nuclei and residual fine vacuolations and reduction in the number of illuminate aggregates. Collectively, Spirulina platensis supplementation could overcome AlCl3-induced neurodegenerative disorder by abolishing oxidative tissue injuries. [ABSTRACT FROM AUTHOR]

Hydroxyapatite nanoparticles (HAP-NPs) are an inorganic component of natural bone and are mainly used in the tissue engineering field due to their bioactivity, osteoconductivity, biocompatibility, non-inflammatory, and non-toxicity properties. However, the current toxicity data for HAP-NPs regarding human health are limited, and only a few results from basic studies have been published. Therefore, the present study was designed to investigate the beneficial role of chitosan nanoparticles (CsNPs) and curcumin nanoparticles (CurNPs) in alleviating nephrotoxicity induced by HAP-NPs in male rats. The results showed that HAP-NPs caused a reduction in antioxidant enzymes and induced lipid peroxidation, nitric oxide production and DNA oxidation. Moreover, HAP-NP administration was associated with intense histologic changes in kidney architecture and immunoreactivity to proliferating cell nuclear antigen (PCNA). However, the presence of CsNPs and/or CurNPs along with HAP-NPs reduced the levels of oxidative stress through improving the activities of antioxidant enzymes. Also, the rats administered the nanoparticles showed a moderate improvement in glomerular damage which matched that of the control group and showed mild positive reactions to PCNA–ir in glomeruli and renal tubules in the cortical and medullary portions. These novel insights confirm that the presence of chitosan and curcumin in nanoforms has powerful biological effects with enhanced bioactivity and bioavailability phenomena compared to their microphase counterparts. Also, they were able to ameliorate the nephrotoxicity induced by HAP-NPs. [ABSTRACT FROM AUTHOR]

The 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is an environmental contaminant toxicant that mediates carcinogenic effects associated with oxidative DNA damage. Docosahexaenoic acid (DHA) with antioxidant functions has many biochemical, cellular, and physiological functions for cells. The present study assessed, for the first time, the ameliorative effect of DHA in alleviating the toxicity of TCDD on primary cultured rat hepatocytes (HEPs). In vitro, isolated HEPs were incubated with TCDD (5 and 10 μM) in the presence and absence of DHA (5, 10, and 20 μM) for 48 h. The cell viability was detected by 3-(4,5-dimethylthiazol-2-yl) 2,5-diphenyltetrazolium bromide (MTT) assay and lactate dehydrogenase (LDH) release. DNA damage was analyzed by liver micronucleus assay and 8-oxo-2-deoxyguanosine (8-OH-dG) level. In addition, total antioxidant capacity (TAC) and total oxidative stress (TOS) were assessed to determine the oxidative injury in HEPs. The results of MTT and LDH assays showed that TCDD decreased cell viability but not DHA. On the basis of increasing treatment concentrations, the dioxin caused significant increases of micronucleated HEPs and 8-OH-dG as compared to control culture. TCDD also led to significant increases in TOS content. On the contrary, in cultures treated with DHA, the level of TAC was significantly increased during treatment in a concentration-dependent fashion. DHA showed therapeutic potential against TCDD-mediated cell viability and DNA damages. As conclusion, this study provides the first evidence that DHA has protective effects against TCDD toxicity on primary cultured rat hepatocytes. [ABSTRACT FROM AUTHOR]

ABSTRACT The present study was designed to investigate genotoxic and cytotoxic effects and oxidative damage of increasing concentrations of nano-hydroxyapatite (5, 10, 20, 50, 75, 100, 150, 300, 500 and 1000 ppm) in primary human blood cell cultures. Cell viability was detected by [3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide] assay and lactate dehydrogenase release, while total antioxidant capacity and total oxidative stress levels were determined to evaluate the oxidative injury. The DNA damage was also analyzed by sister chromatid exchange, micronuclei, chromosome aberration assays and 8-oxo-2-deoxyguanosine level as indicators of genotoxicity. The results of [3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide] and lactate dehydrogenase assays showed that the higher concentrations (150, 300, 500 and 1000 ppm) of hydroxyapatite nanoparticles (HAP NPs) decreased cell viability. HAP NPs led to increases of total oxidative stress (300, 500 and 1000 ppm) levels and decreased total antioxidant capacity (150, 300, 500 and 1000 ppm) levels in cultured human blood cells. On the basis of increasing concentrations, HAP NPs caused significant increases of sister chromatid exchange, micronuclei, chromosome aberration rates and 8-oxo-2-deoxyguanosine levels as compared to untreated culture. In conclusion, the obtained in vitro results showed that HAP NPs had dose-dependent effects on inducing oxidative damage, genotoxicity and cytotoxicity in human blood cells. Copyright © 2013 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

The purpose of this study was to evaluate the effect of carotenoid astaxanthin (ASTA) on cultured primary rat hepatocytes treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the cell viability (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide, MTT), lactate dehydrogenase (LDH) activity, 8-oxo-2-deoxyguanosine (8-OH-dG), total antioxidant capacity (TAC), and total oxidative stress (TOS) levels, and liver micronucleus rates. ASTA (2.5, 5, and 10 µM) was added to cultures alone or simultaneously with TCDD (5 and 10 µM) for 48 h. The results of MTT and LDH assays showed that both doses of TCDD caused significant decrease in cell viability. Also, TCDD significantly increased TOS and decreased TAC level in rat hepatocytes. On the basis of increasing doses, the dioxin caused significant increase in micronucleated hepatocytes) and 8-OH-dG level as compared to control culture. The presence of ASTA with TCDD minimized its effects on primary hepatocytes cultures and DNA damages. [ABSTRACT FROM PUBLISHER]

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induces hepatic damage. Propolis exhibits antioxidant properties and several studies suggest that supplementations with antioxidants can influence hepatotoxicity. Therefore, the aim of the current study was to explore the effectiveness of propolis in alleviating the toxicity of TCDD in the liver of rats. Animals were divided into six groups, namely, TCDD (0.75 and 8 µg/kg body weight (bw)), propolis (50 mg/kg bw), TCDD (0.75 and 8 µg) plus propolis (50 mg/kg bw), and control, respectively. Rats were intraperitoneally administered with their respective doses daily for 21 days. In rats that received a high dose of TCDD, the antioxidant enzymes were significantly decreased and the serious pathological findings were established. Also, the rate of hepatocyte micronucleus (HMN) was increased after treating with TCDD. The reactions of enzymes in control and low-dose group were weak. The frequencies of HMN and liver histology were similar to both the groups. The presence of propolis with TCDD alleviated its pathological effects in hepatic tissue. Propolis also prevented the suppression of antioxidant enzymes in the livers of animals exposed to TCDD and displayed a strong protective effect against HMN. It can be concluded that propolis has beneficial influences and was able to antagonize TCDD toxicity in the liver. [ABSTRACT FROM PUBLISHER]

Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) represents a potential health risk and hepatotoxicity. Astaxanthin (ASTA) exhibits antioxidant properties and can influence hepatotoxicity. Therefore, the present study was carried out for using ASTA against hepatotoxicity induced by TCDD in the liver of rats. Animals were treated intraperitoneally daily with TCDD (8 µg/kg body weight (b.w.)), ASTA (12.5 mg/kg b.w. and 25 mg/kg b.w.) and TCDD plus ASTA (12.5 and 25 mg/kg b.w.) for 21 days. TCDD significantly decreased the activities of antioxidant enzymes and resulted in serious pathological findings. Moreover, the rate of micronucleus (MN) in hepatocytes increased after treating with TCDD. The activities of enzymes, frequencies of MNs and liver histology in lower dosage group of ASTA remained unchanged compared with the control group. In rats treated with ASTA, at higher dosage alone, the MNs remained unchanged and the activities of antioxidant enzymes significantly increased. The presence of ASTA (except for lower dose) with TCDD alleviated its pathological effects in hepatic tissue. ASTA also prevented the suppression of antioxidant enzymes in the livers of animals exposed to TCDD and displayed a strong protective effect against MNs. Thus, the present findings might provide new insight into the development of therapeutic and preventive approaches of TCDD toxicity. [ABSTRACT FROM AUTHOR]

The aim of this study was to explore the effectiveness of l-glutamine (Gln) in alleviating the toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in liver of rats. Rats were intraperitoneally administered Gln and TCDD doses daily for 21 days. In the liver of rats, the biochemical tests, pathological examination and micronucleus (MN) test were performed. TCDD significantly decreased the activities of antioxidant enzymes and serious pathological findings. Moreover, the rate of MNs in hepatocytes increased after treatment with dioxin. In rats treated with Gln alone, the MNs remained unchanged, but the ratio of glutathione (GSH) and the activity of glutathione peroxidase (GSH-Px) were significantly increased. Gln also prevented the suppression of GSH-Px (except for superoxide dismutase and catalase) and GSH in the livers of animals exposed to TCDD and displayed a strong protective effect against MNs. Thus, our findings for Gln might provide new insight into the development of therapeutic and preventive approaches in TCDD toxicity. [ABSTRACT FROM AUTHOR]

Abstract: The present experiment was undertaken to determine the effectiveness of propolis in alleviating the toxicity of TCDD on cultured primary rat hepatocytes. Propolis (25, 50 and 100μM) was added to plain culture or simultaneously with TCDD (5 and 10μM). The hepatocytes were treated with TCDD and propolis for 48h. Then cell viability was detected by [3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide] (MTT) assay and lactate dehydrogenase (LDH) release, while total antioxidant capacity (TAC) and total oxidative stress (TOS) levels were determined to evaluate the oxidative injury. The DNA damage was also analyzed by liver micronucleus assay (LMN) and 8-oxo-2-deoxyguanosine (8-OH-dG). The results of MTT and LDH assays showed that TCDD decreased cell viability. TCDD also increased TOS level and decreased TAC level in rat hepatocytes. On the basis of increasing doses, the TCDD caused significant increases of micronucleated hepatocytes (MNHEPs) and 8-OH-dG levels as compared to control culture. In cultures treated with propolis alone, cell viability and TOS level were not affected, while the level of TAC was significantly increased in dose-dependent fashion. The presence of propolis with TCDD modulated its toxic effects on primary hepatocytes cultures. Noteworthy, propolis has a protective effect against TCDD-mediated DNA damages. [Copyright &y& Elsevier]

Abstract: The present study was carried out to evaluate the potential protective role of quercetin and curcumin against paracetamol-induced oxidative injury, liver damage and impairment of kidney function, as well as haematotoxicity in rats. Also, N-acetylcysteine was used to evaluate the potency of quercetin and curcumin. Paracetamol caused an elevation in thiobarbituric acid-reactive substances (TBARS) paralleled with significant decline in glutathione peroxidase, glutathione S-transferase, superoxide dismutase and catalase activities (in plasma, brain, lung, heart, liver, kidney and testes) and glutathione content (in lung, liver and kidney). The apparent oxidative injury was associated with evident hepatic necrosis confirmed in histological examination, elevated plasma transmainases, alkaline phosphatase and lactate dehydrogenase. Paracetamol reduced plasma total protein, albumin and globulin, while increased bilirubin, urea and creatinine, and induced haematotoxicity. The presence of quercetin or curcumin with paracetamol successfully mitigated the rise in TBARS and restored the activities of antioxidant enzymes compared to the group treated with both paracetamol and N-acetylcysteine. They also protected liver histology, normalized liver and kidney functions, which was more pronounced with curcumin. Therefore, it can be concluded that concomitant administration of quercetin or curcumin with paracetamol may be useful in reversing the toxicity of the drug compared to N-acetylcysteine. [ABSTRACT FROM AUTHOR]

Abstract: Aluminium is present in several manufactured foods and medicines and is also used in water purification. Therefore, the present experiment was undertaken to determine the effectiveness of propolis in modulating the aluminium chloride (AlCl3) induced genotoxicity and hepatotoxicity in liver of rats. Animals were assigned to 1 of 4 groups: control; 34mg AlCl3/kg bw; 50mg propolis/kg bw; AlCl3 (34mg/kg bw) plus propolis (50mg/kg bw), respectively. Rats were orally administered their respective doses daily for 30days. At the end of the experiment, rats were anesthetized and hepatocytes (HEP) were isolated for counting the number of micronucleated hepatocytes (MNHEPs). In addition, the levels of serum enzymes and histological alterations in liver were investigated. AlCl3 caused a significant increase in MNHEPs, alkaline phosphatase, transaminases (AST and ALT) and lactate dehydrogenase (LDH). Furthermore, severe pathological damages such as: sinusoidal dilatation, congestion of central vein, lipid accumulation and lymphocyte infiltration were established in liver. On the contrary, treatment with propolis alone did not cause any adverse effect on above parameters. Moreover, simultaneous treatments with propolis significantly modulated the toxic effects of AlCl3. It can be concluded that propolis has beneficial influences and could be able to antagonize AlCl3 toxicity. [Copyright &y& Elsevier]

Abstract: The current study was carried out to elucidate the modulating effect of chicory (Cichorium intybus L.)-supplemented diet against nitrosamnine-induced oxidative stress and hepatotoxicity in male rats. Rats were divided into four groups and treated for 8weeks as follow: group 1 served as control; group 2 fed on chicory-supplemented diet (10% w/w); group 3 received simultaneously nitrosamine precursors [sodium nitrite (0.05% in drinking water) plus chlorpromazine (1.7mg/kg body weight)] and group 4 received nitrosamine precursors and fed on chicory-supplemented diet. The obtained results revealed that rats received nitrosamine precursors showed a significant increase in liver TBARS and total lipids, total cholesterol, bilirubin, and enzymes activity (AST, ALT, ALP and γ-GT) in both serum and liver. While a significant decrease in the levels of GSH, GSH-Rx, SOD, catalase, total protein and albumin was recorded. On the other hand, chicory-supplemented diet succeeded to modulate these observed abnormalities resulting from nitrosamine compounds as indicated by the reduction of TBARS and the pronounced improvement of the investigated biochemical and antioxidant parameters. So, it could be concluded that chicory has a promising role and it worth to be considered as a natural substance for ameliorating the oxidative stress and hepatic injury induced by nitrosamine compounds. [Copyright &y& Elsevier]

Abstract: Triphenyltin (TPT) is known to cause endocrine disruption, reproductive toxicity and a decrease in testosterone production. It is involved in the production of reactive oxygen species. Propolis has been reported to be an important antioxidant. Therefore, the present study aimed to elucidate the possible protective effects of propolis in alleviating the toxicity of triphenyltin chloride (TPTCl) on reproductive performance, testosterone levels, lipid peroxidation and enzyme activities in seminal plasma of male New Zealand white rabbits. Animals were orally administered the doses of propolis, TPTCl and propolis plus TPTCl every day for 12weeks. Results showed that semen quality was deteriorated following treatment with TPTCl. Also, testosterone levels, body weight (BW), relative weights of testes (RWT) and epididymis (RWE) were decreased. Thiobarbituric acid-reactive substances and lactate dehydrogenase were increased, while glutathione S-transferase, transaminases and phosphatases were decreased in seminal plasma of rabbits treated with TPTCl compared to control. Propolis alone significantly increased testosterone levels, BW, RTW, REW, semen characteristics and seminal plasma enzymes, and decreased the levels of free radicals and lactate dehydrogenase. Furthermore, the presence of propolis with TPTCl alleviates its toxic effects. From the present study, it can be concluded propolis can be effective in the protection of TPTCl-induced reproductive toxicity. [Copyright &y& Elsevier]

Abstract: The objective of the current study was to analyze the reproductive toxicity caused by lambda-cyhalothrin (LCT) in male rabbits, and to evaluate the possible protective effect of vitamin E (Vit. E) as antioxidant. Animals were orally administered their respective doses of LCT every other day and given drinking water supplemented with vitamin E for 16weeks. Results showed that semen quality was deteriorated following treatment with LCT. Also, testosterone levels, body weight (BW), feed intake (FI), and relative testes (RTW) and epididymis (REW) weights were significantly decreased. Concentrations of thiobarbituric acid-reactive substances (TBARS) were significantly increased in seminal plasma of rabbits treated with LCT compared with control. While, activities of glutathione S-transferase (GST), transaminases and acid phosphatase (AcP) were significantly decreased. Vitamin E alone significantly increased testosterone levels, BW, FI, RTW, REW, semen characteristics and seminal plasma enzymes, and decreased the levels of TBARS. Also, the present study showed that vitamin E might be effective against LCT-induced reproductive toxicity. It was suggested that LCT exerted a significant adverse effect on reproductive performance of male rabbits. Furthermore, vitamin E antagonized the toxic effects of LCT and improved semen quality of male rabbit. [Copyright &y& Elsevier]

Abstract: Fluorosis is a serious public health problem in many parts of the world. As in the case of many chronic degenerative diseases, increased production of reactive oxygen species has been considered to play an important role, even in the pathogenesis of chronic fluoride toxicity. Black berry is closely linked to its protective properties against free radical attack. Therefore, the aim of this study was to demonstrate the role of black berry juice (BBJ) in decreasing the hepatotoxicity and oxidative stress of sodium fluoride (NaF). Results showed that NaF caused elevation in liver TBARS and nitric oxide (NO), and reduction in superoxide dismutase (SOD), catalase (CAT), total antioxidant capacity (TAC) and glutathione (GSH). Plasma transaminases (AST and ALT), creatine kinase (CK), lactate dehydrogenase (LDH), total lipids (TL), cholesterol, triglycerides (TG), and low density lipoprotein–cholesterol (LDL–c) were increased, while high density lipoprotein–cholesterol (HDL–c) was decreased. On the other hand, BBJ reduced NaF-induced TBARS, NO, TL, cholesterol, TG, LDL–c, AST, ALT, CK and LD. Moreover, it ameliorated NaF-induced decrease in SOD, CAT, GSH, TAC and HDL–c. Therefore, the present results revealed that BBJ has a protective effect against NaF-induced hepatotoxicity by antagonizing the free radicals generation and enhancement of the antioxidant defence mechanisms. [Copyright &y& Elsevier]

Abstract: Different forms of aluminium (Al) are environmental xenobiotics that induce free radical-mediated cytotoxicity and reproductive toxicity. Propolis has been reported to be important antioxidant. Therefore, this study aimed at elucidating the protective effects of propolis against reproductive toxicity of aluminium chloride (AlCl3) in male rats. The first group served as control. Group 2 received 34mg AlCl3/kg bw (1/25 LD50). Group 3 was administered 50mg propolis/kg bw/day. Group 4 was treated with AlCl3 plus propolis. Treatment was continued for 70days. AlCl3 caused a decrease in testes, seminal vesicle and epididymis weights, sperm concentration, motility, testosterone level and the activities of 17-ketosteroid reductase, CAT and GST, and GSH content. While, dead and abnormal sperm and testes TBARS concentrations were increased. In the AlCl3-treated group, histopathologic examinations revealed apparent alterations in the testes, where it induced marked lesions in seminiferous tubules. Propolis alone decreased dead and abnormal sperm and TBARS, and increased testosterone, GSH, 17-ketosteroid reductase, CAT and GST. Results showed that propolis antagonized the harmful effects of AlCl3. This was proved histopathologically by the great improvement in testes. In conclusion propolis could be effective in the protection against the reproductive toxicity of AlCl3. [Copyright &y& Elsevier]

Abstract: The present study was conducted to investigate the antioxidative effect of curcumin against sodium arsenite-induced oxidative damage in rat. Animals were divided into four groups, the first group was used as control. Groups 2, 3 and 4 were orally treated with curcumin (15mg/kg BW), sodium arsenite (Sa, 5mg/kg BW) and sodium arsenite plus curcumin, respectively. Rats were orally administered their respective doses daily for 30days. Results showed that Sa increased thiobarbituric acid-reactive substances (TBARS) in plasma, liver, kidney, lung, testes and brain. While, the activities of glutathione S-transferase, superoxide dismutase and catalase and the content of sulfhydryl groups (SH-groups) were significantly decreased in plasma and tissues compared to control. Treatment with curcumin alone reduced the levels of TBARS, while induced the activities of the antioxidant enzymes, and the levels of SH-groups. The presence of curcumin with Sa reduced the induction in the levels of TBARS and induced the decrease in the activities of antioxidant enzymes and the levels of SH-groups. Results indicated that treatment with Sa decreased body weight and increased liver weight compared to control. The presence of curcumin with Sa alleviated its toxic effects. It can be concluded that curcumin has beneficial influences and could be able to antagonize Sa toxicity. [Copyright &y& Elsevier]

Abstract: The present study was undertaken to evaluate the therapeutic efficacy of curcumin in terms of normalization of altered biochemical parameters following sodium arsenite treatment in rats. Animals were divided into four groups. The first group was used as control. While, groups 2, 3 and 4 were orally treated with curcumin (Cur, 15mg/kg BW), sodium arsenite (Sa, 5mg/kg BW) and sodium arsenite plus curcumin, respectively. Results showed that the activities of transaminases and phosphatases were significantly decreased in liver due to Sa administration, whereas increased in plasma. The activity of brain and plasma acetylcholinesterase (AChE) was decreased in rats treated with Sa. Also, Sa significantly decreased plasma total protein (TP), albumin (Alb) and high density lipoprotein-cholesterol (HDL-c), while increased glucose, urea, creatinine, bilirubin, total lipid (TL), cholesterol, triglyceride (TG) and low density lipoprotein-cholesterol (LDL-c). Curcumin alone decreased the levels of glucose, urea, creatinine, TL, cholesterol, TG and LDL-c. Curcumin reduced Sa-induced transaminases, phosphatases, glucose, urea, creatinine, bilirubin, TL, cholesterol and TG. Moreover, curcumin induced Sa-reduced liver transaminases and phosphatases, plasma and brain AChE, and the levels of TP and Alb. Experimental results, therefore suggested that curcumin protects arsenic induced biochemical alterations in rats. [Copyright &y& Elsevier]

Abstract: An in vitro study using rabbit sperm was designed to evaluate the cytotoxic effects of different concentrations of aluminium chloride (AlCl3) at 0, 2 and 4h of incubation on sperm motility and viability, oxidative status and the activities of some antioxidant enzymes (superoxide dismutase (SOD) and catalase (CAT)), transaminases and acid phosphatase. The role of vitamin C (1mM) or vitamin E (2mM) was also investigated in counteracting deterioration caused by AlCl3 on the tested parameters. Rabbit sperm was incubated with different concentrations of AlCl3 (0, 1, 5, 10, 15 and 20mM) with or without vitamin C or vitamin E for 2 and 4h. Results revealed that the percentage of motile and viable sperm decreased significantly after AlCl3 treatment at 10, 15 and 20mM and the response was both concentration and time dependent. Aluminium chloride at concentrations of 10, 15 and 20mM caused significant induction of oxidative stress as evidenced by increased thiobarbituric acid reactive substances (TBARS) levels and inhibition in the activities of SOD and CAT. Increase in the activities of aspartate transaminase (AST) and alanine transaminase (ALT) and decline in the activity of acid phosphatase (ACP) were also observed at AlCl3 concentrations of 15 and 20mM. Co-incubation with either vitamin C or vitamin E resulted in marked degrees of protection against AlCl3-induced cytotoxic effects, represented in decreased TBARS levels and restoration of enzymes activities near control. On the other hand, no significant effect was exerted from vitamin C or vitamin E on motility and viability. The present study demonstrated that AlCl3 caused deterioration in sperm motility and viability, enhancement of free radicals and alterations in enzymes activities. The antioxidants revealed protective effects against the cytotoxicity of AlCl3. [Copyright &y& Elsevier]

Abstract: Deltamethrin is a synthetic pyrethroid insecticide used worldwide in agriculture, home pest control, protection of foodstuff and disease vector control. The objective of this study was to investigate the propensity of deltamethrin to induce oxidative stress and changes in biochemical parameters and enzyme activities in male rats following a short-term (30 days) oral exposure and its possible attenuation by Vitamin E (Vit. E). Rats were assigned to 1 of 4 treatment groups: 0mg Vit. E and 0mg deltamethrin/kg body weight (BW) (control); 100mg Vit. E/kg BW; 1.28mg deltamethrin/kg BW; 100mg Vit. E plus 1.28mg deltamethrin/kg BW. Results obtained showed that deltamethrin significantly (P <0.05) induced thiobarbituric acid-reactive substances (TBARS; the marker of lipid peroxidation) in plasma. The activities of glutathione S-transferase (GST) and superoxide dismutase (SOD) were significantly decreased due to deltamethrin administration. On the other hand, treatment with Vitamin E alone increased the activities of GST and SOD, and decreased the levels of TBARS. Also, Vitamin E alleviated the harmful effect of deltamethrin in the combination group. Enzymatic activities of aminotransferases (AST and ALT), phosphatases (AcP and AlP) and lactate dehydrogenase (LDH) in plasma were significantly increased, while acetylcholinesterase (AChE) was inhibited. Deltamethrin significantly (P <0.05) increased the levels of plasma total lipid (TL), cholesterol, triglyceride (TG), low density lipoprotein (LDL) and very low density lipoprotein (VLDL), while the level of high density lipoprotein (HDL) decreased. Vitamin E alone decreased the levels of lipids and lipoproteins, and alleviated the harmful effects of deltamethrin. Concentrations of glucose, urea, creatinine and total bilirubin were increased. While, plasma total protein (TP), albumin (A) and globulin (G) were significantly (P <0.05) decreased. The present study revealed that the presence of Vitamin E could diminish the adverse effects of deltamethrin on most of biochemical parameters, lipid peroxidation and enzyme activities in rats. [Copyright &y& Elsevier]

Abstract: Aluminium (Al) has been proposed as an environmental factor that may contribute to some diseases, affect several enzymes and other biomolecules and induced free radical-mediated cytotoxicity. Also, Al induced reproductive toxicity and exerted a significant adverse effect on the steroidogenesis. The antioxidant ascorbic acid (AA) plays an important role in various physiological processes in the body including detoxification of different toxic materials. Therefore, the present investigation aimed to elucidate possible protective effects of AA in alleviating the toxicity of aluminium chloride (AlCl3) on reproductive performance, lipid peroxidation and enzyme activities in seminal plasma of male New Zealand white rabbits. Six rabbits per group were assigned to one of four treatment groups: 0mg AA and 0mg AlCl3/kg body weight (BW) (control); 40mg AA/kg BW; 34mg AlCl3/kg BW; 34mg AlCl3 plus 40mg AA/kg BW. Rabbits were orally administered their respective doses every other day for 16 weeks. Results obtained showed that AlCl3 significantly (P <0.05) decreased libido (by increasing the reaction time), ejaculate volume, sperm concentration, total sperm output, sperm motility (%), total motile sperm per ejaculate (TMS), packed sperm volume (PSV), total functional sperm fraction (TFSF), normal and live sperm and semen initial fructose. While initial hydrogen ion concentration (pH) and dead and abnormal sperm were increased (P <0.05). Live body weight (LBW), feed intake (FI) and relative weights of testes (RTW) and epididymis (REW) were significantly (P <0.05) decreased. Concentrations of thiobarbituric acid-reactive substances (TBARS) were significantly (P <0.05) increased in seminal plasma of rabbits treated with AlCl3 compared with control. While, activities of glutathione S-transferase (GST), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and acid phosphatase (AcP) were significantly (P <0.05) decreased. Ascorbic acid alone significantly increased LBW, FI, RTW, REW, semen characteristics and seminal plasma enzymes, and decreased the levels of free radicals. Also, the present study showed that ascorbic acid might be effective in the protection of aluminium-induced reproductive toxicity. It was suggested that AlCl3 exerted a significant adverse effect on reproductive performance of male rabbits. Furthermore, AA could be able to antagonize the toxic effects of AlCl3 and improved semen quality of male rabbit. [Copyright &y& Elsevier]

Abstract: The objective of this study was to determine the protective role of ascorbic acid (AA, 40mg/kg BW) on reproductive performance of male New Zealand White rabbits given sublethal dose (20mg/kg BW every other day for 12 weeks) of stannous chloride (SnCl2). Results showed that treatment with SnCl2 caused a decrease (P<0.05) in libido (by increasing the reaction time), ejaculate volume, sperm concentration, total sperm output, sperm motility (%), total motile sperm per ejaculate (TMS), packed sperm volume (PSV), total functional sperm fraction (TFSF), normal and live sperm and semen initial fructose. Dead sperm and initial hydrogen ion concentration (pH) were increased. While, relative weights of testes (RTW) and epididymis (REW) were decreased. On the other hand, live body weight (LBW) and dry matter intake (DMI) did not change. Treatment with AA alone caused significant increase in LBW, DMI, RTW, REW and semen characteristics compared to control group. Also, the presence of AA with SnCl2 minimized its harmful effects. Results obtained revealed suggest that assessment of reproductive toxicity of stannous chloride needs to be addressed, and may presently be underestimated. Also, the beneficial influences of AA in counteracting the toxic effects of SnCl2 and improved the reproductive performance of male rabbit was demonstrated. [Copyright &y& Elsevier]

The objective of this study was to determine the effect of either 2.5 mg/kg Body Weight or 5 mg/kg Body Weight (BW) doses of isoflavones on semen quality, testosterone levels, lipid peroxidation and semen biochemistry of male New Zealand White rabbits. Animals were given both 2.5 mg/kg BW and 5 mg/kg BW doses of isoflavones. The tested doses were given to rabbits orally every other day for 13 weeks. Treatment with isoflavones caused an increase (p < 0.05) in libido (by decreasing the reaction time), sperm concentration, sperm motility (%), total motile sperm per ejaculate (TMS), packed sperm volume (PSV), total functional sperm fraction (TFSF), total sperm output, initial fructose concentration and normal sperm, while dead sperm was reduced compared to control animals. On the other hand, ejaculate volume, initial hydrogen ion concentration (pH) and plasma testosterone levels did not change in treated animals with both doses of isoflavones as compared to control. Concentrations of thiobarbituric acid-reactive substances (TBARS), total lipids, and low density lipoprotein were significantly (p < 0.05) reduced in seminal plasma of rabbits treated with either 2.5 mg/kg BW or 5 mg/kg BW doses of isoflavones. While, the activities of glutathione S-transferase (GST), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), acid phosphatase (AcP), and alkaline phosphatase (AlP) were significantly (p < 0.05) increased in seminal plasma of treated animals. Also, total cholesterol, percentage cholesterol (out of total lipids), and high density lipoprotein were significantly (p < 0.05) increased, while triglyceride did not change in seminal plasma of treated animals. Supplementation at either level of isoflavones did not cause changes in live body weight (LBW), dry matter intake (DMI), and relative weights of testes and epididymis. The present results showed that either 2.5 mg/kg BW or 5 mg/kg BW doses of isoflavones caused an improvement of some semen characteristics and did not have negative effects on male fertility. [ABSTRACT FROM AUTHOR]

For a long time, aluminium (Al) has been considered an indifferent element from a toxicological point of view. In recent years, however, Al has been implicated in the pathogenesis of several clinical disorders, such as dialysis dementia, the fulminant neurological disorder that can develop in patients on renal dialysis. Therefore, the present experiment was carried out to determine the effectiveness of l-ascorbic acid (AA) in alleviating the toxicity of aluminium chloride (AlCl3) on certain hemato-biochemical parameters, lipid peroxidation and enzyme activities of male New Zealand white rabbits. Six rabbits per group were assigned to 1 of 4 treatment groups: 0 mg AA and 0 mg AlCl3/kg body weight (BW) (control); 40 mg AA/kg BW; 34 mg AlCl3/kg BW (1/25 LD50); 34 mg AlCl3 plus 40 mg AA/kg BW. Rabbits were orally administered their respective doses every other day for 16 weeks. Evaluations were made for lipid peroxidation, enzyme activities and hemato-biochemical parameters. Results obtained showed that AlCl3 significantly (P<0.05) induced free radicals and decreased the activity of glutathione S-transferase (GST) and the levels of sulfhydryl groups (SH groups) in rabbit plasma, liver, brain, testes and kidney. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AlP), acid phosphatase (AcP), and phosphorylase activities were significantly decreased in liver and testes due to AlCl3 administration. While, plasma, liver, testes and brain lactate dehydrogenase (LDH) activities were significantly increased. Contrariwise, the activity of acetylcholinesterase (AChE) was significantly decreased in brain and plasma. Aluminium treatment caused a significant decrease in plasma total lipids (TL), blood haemoglobin (Hb), total erythrocytic count (TEC) and packed cell volume (PCV), and increased total leukocyte count (TLC) and the concentrations of glucose, urea, creatinine, bilirubin and cholesterol. Ascorbic acid alone significantly decreased the levels of free radicals, TL, cholesterol, glucose and creatinine, and increased the activity of GST, SH groups, Hb, TEC and PCV. While, the rest of the tested parameters were not affected. Also, the present study showed that ascorbic acid can be effective in the protection of aluminium-induced toxicity. [Copyright &y& Elsevier]

Triphenyltin (TPT) is known to cause endocrine disruption, reproductive toxicity and a decrease in testosterone production. It is involved in the production of reactive oxygen species. Propolis has been reported to be an important antioxidant. Therefore, the present investigation aimed to elucidate the possible protective effects of propolis in alleviating the toxicity of triphenyltin chloride (TPTCl) on reproductive performance, testosterone levels, lipid peroxidation and enzyme activities in seminal plasma of male New-Zealand white rabbits. Six rabbits per group were assigned to 1 of 4 treatment groups: 0 mg propolis and 0 mg TPTCl/kg bw (control); 50 mg propolis/kg bw; 0.5 mg TPTCl/kg bw; 0.5 mg TPTCl plus 50 mg propolis/kg bw, respectively. Rabbits were orally administered their respective doses every day for 12 weeks. Results showed that semen quality was deteriorated following treatment with TPT. It significantly (P<0.05) decreased libido (by increasing the reaction time), ejaculate volume, sperm concentration, total sperm output, sperm motility (%), total motile sperm per ejaculate (TMS), packed sperm volume (PSV), total functional sperm fraction (TFSF), normal and live sperm and semen initial fructose. While, initial hydrogen ion concentration (pH), and dead sperm were increased. Also, testosterone levels, body weight (BW), relative weights of testes (RTW) and epididymis (REW) were decreased. Levels of thiobarbituric acid-reactive substances and lactate dehydrogenase were increased, while the activities of glutathione S-transferase, transaminases and phosphatases were decreased in seminal plasma of rabbits treated with TPTCl compared to control. Propolis alone significantly increased testosterone levels, BW, RTW, REW, semen characteristics and seminal plasma enzymes, and decreased the levels of free radicals and lactate dehydrogenase. Furthermore, the presence of propolis with TPTCl alleviates its toxic effects. Therefore, the present study concluded that propolis can be effective in the protection of TPTCl-induced reproductive toxicity. [ABSTRACT FROM AUTHOR]

Abstract: The protective effect of sesame oil against cypermethrin-induced brain toxicity was studied. Female rats were orally treated with cypermethrin, sesame oil and their combination for 30 consecutive days. The results showed that cypermethrin increased thiobarbituric acid-reactive substances (TBARS), and decreased glutathione (GSH) and the activities of the antioxidant enzymes. Brain injury was confirmed by histopathological changes and DNA damage. Also, the reduction in the activities of acetylcholinesterase and monoamine oxidase (AChE & MAO), total protein, albumin and body weight, and the induction in triacylglycerol and cholesterol have been observed due to cypermethrin toxicity. Animals treated with sesame oil and cypermethrin together showed that brain TBARS and plasma triacylglycerol and cholesterol returned to the control level which indicating a protective effect of sesame oil. Also, sesame oil was able to attenuate the decrease in total protein, albumin, triacylglycerol and cholesterol, GSH, AChE and antioxidant enzymes induced by cypermethrin. In addition, sesame oil protected the brain histological changes and fragmentation of genomic DNA in animals treated with cypermethrin. The present results showed a protective effect of sesame oil against the cypermethrin induced brain toxicity and this could be associated mainly with the attenuation of the oxidative stress and the preservation in antioxidant enzymes. [Copyright &y& Elsevier]

Abstract: This paper studied the possible effect of folic acid in fortified Baladi bread on the prevention of colon cancer development in rats. Wheat flour samples (82% extraction rate) and soy bean flour were analyzed to determine their folic acid contents using the High Performance Liquid Chromatography (HPLC). Unfortified and folic acid fortified Baladi breads were prepared. Samples from each step of bread preparation were analyzed for folic acid concentration. Protein, fat, ash, fibers and carbohydrates percentages were also determined. Rats were divided into five groups, four of them were injected subcutaneously with dimethylhydrazine (DMH). After 15weeks, the rats were sacrificed for pathological examination. Results showed that the folic acid content in wheat flour (82% extraction rate) was found to be highly significantly lower than that in soybean flour. After baking, folic acid content in all breads was found to decrease significantly. The highest protein and fat contents were found in soybean flour fortified Baladi bread. The colons of rats of groups 3 (fed 5% soy flour fortified Baladi bread) and 5 (fed Baladi bread fortified with 5% soy flour+8mg folic acid/kg wheat flour) were the mostly affected by DMH injection as premalignant changes were observed. [Copyright &y& Elsevier]

Abstract: Aluminium is present in many manufactured foods and medicines and is also added to drinking water during purification purposes. Therefore, the present experiment was undertaken to determine the effectiveness of propolis in alleviating the toxicity of aluminium chloride (AlCl3) on biochemical parameters, antioxidant enzymes and lipid peroxidation of male Wistar Albino rats. Animals were assigned to 1 of 4 groups: control; 34mg AlCl3/kg bw; 50mg propolis/kg bw; AlCl3 (34mg/kg bw) plus propolis (50mg/kg bw), respectively. Rats were orally administered their respective doses daily for 70days. The levels of thiobarbituric acid reactive substances (TBARS) was increased, and the activities of glutathione S-transferase, superoxide dismutase, catalase and glutathione peroxidase were decreased in liver, kidney and brain of rats treated with AlCl3. While, TBARS was decreased and the antioxidant enzymes were increased in rats treated with propolis alone. Plasma transaminases, lactate dehydrogenase, glucose, urea, creatinine, bilirubin, total lipid, cholesterol, triglyceride and LDL-c were increased, while total protein, albumin and high HDL-c were decreased due to AlCl3 administration. The presence of propolis with AlCl3 alleviated its toxic effects in rats treated with AlCl3. It can be concluded that propolis has beneficial influences and could be able to antagonize AlCl3 toxicity. [Copyright &y& Elsevier]

This study was conducted to investigate the protective potential of a pharmaceutically formulated capsule of artichoke leaf powder (ArLP) against aflatoxin B 1 (AFB 1 )-induced hepatotoxicity in male albino rats. In the 42-day experiment, rats were divided into five equal groups: (i) control, treated with sterile water, (ii) treated with 4% DMSO as AFB 1 vehicle, (iii) ArLP of 100 mg kg -1 bw, (iv) AFB 1 of 72 µg kg -1 bw, and (v) AFB 1 plus ArLP. Exposure of rats to AFB 1 resulted in hepatotoxicity as manifested by the intensification of oxidative stress, production of free radicals and significant increase in the activity levels of liver function enzymes relative to the control. Significant reductions in both the enzymatic and non-enzymatic antioxidant markers as well as histopathological abnormalities in liver tissues were also observed. Notably, the combined administration of ArLP with AFB 1 clearly reduced AFB 1 -mediated adverse effects leading to the normalization of most of these parameters back to control levels. These findings clearly highlight the potential benefits of artichoke dietary supplements as a safe and natural solution in counteracting the adverse hepatotoxic effects conferred by AFB 1 exposure. Further research is warranted to fully dissect the biochemical and molecular mechanism of action of the observed artichoke-mediated hepatoprotection.

The involvement of reactive oxygen species (ROS) has been implicated in the toxicity of various pesticides. Our study was designed to investigate the induction of oxidative stress by cypermethrin; a Type II pyrethroid in rat liver and kidney. In addition, the protective role of sesame oil against the toxicity of cypermethrin was investigated. Animals were divided into four equal groups; the first group used as control while groups 2, 3 and 4 were treated with sesame oil (5 mL/kg b.w), cypermethrin (12 mg/kg b.w) and the combination of both sesame oil (5 mL/kg b.w) plus cypermethrin (12 mg/kg b.w), respectively. Rats were daily administered with their respective doses for 30 days by gavage. Repeated oral administration of cypermethrin was found to reduce the level of glutathione (GSH) and the activities of the antioxidant enzymes. While, the level of TBARS was elevated indicating the presence of oxidative stress. The activities of LDH, AST and ALT were decreased in the liver extract while increased in the plasma of the cypermethrin-treated group. Also, the levels of urea and creatinine were significantly increased after treatment with cypermethrin. Liver and kidney injury was confirmed by the histological changes. In conclusion, the administration of sesame oil provided significant protection against cypermethrin-induced oxidative stress, biochemical changes, histopathological damage and genomic DNA fragmentation.

Deleterious effects of chromium (VI) compounds are diversified affecting almost all the organ systems in a wide variety of animals. Therefore, the present study was carried out to determine the effectiveness of folic acid (FA) in alleviating the toxicity of chromium (VI) on certain biochemical parameters, lipid peroxidation, and enzyme activities of male New Zealand white rabbits. Six rabbits per group were assigned to one of four treatment groups: 0 mg FA and 0 mg Cr(VI)/kg BW (control); 8.3 microg FA/kg BW; 5 mg Cr(VI)/kg BW; 5 mg Cr(VI) plus 8.3 microg FA/kg BW, respectively. Rabbits were orally administered their respective doses every day for 10 weeks. Results obtained showed that Cr(VI) significantly (P < 0.05) increased the levels of free radicals and the activity of glutathione S-transferase (GST), and decreased the content of sulfhydryl groups (SH groups) in liver, testes, brain, kidney, and lung. The activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AlP), acid phosphatase (AcP), and lactate dehydrogenase (LDH) were significantly decreased in liver and testes due to Cr(VI) administration. Also, AlP and AcP activities were significantly decreased in kidney and lung. The activity of acetylcholinesterase (AChE) was significantly decreased in brain and plasma. Contrariwise, the activities of AST and ALT were significantly increased in plasma, while AlP and AcP decreased. Chromium (VI) treatment caused a significant decrease in plasma total protein (TP) and globulin, and increased total lipids (TL), cholesterol, glucose, urea, creatinine, and bilirubin concentrations. Folic acid alone significantly decreased the levels of free radicals in liver, brain, and kidney, and increased the content of SH-group. The activities of AST, ALT, and LDH in liver; AST, ALT, AlP, AcP, and LDH in testes; AcP in kidney; AlP and AcP in lung, and LDH in brain were significantly increased. Plasma TP and albumin were increased, while urea and creatinine were decreased. The presence of FA with Cr(VI) restored the changes in enzyme activities and biochemical parameters. In conclusion, folic acid could be effective in the protection of chromium-induced toxicity.