Chlorpyrifos acute exposure induces hyperglycemia and hyperlipidemia in rats

In this study we evaluated the hyperglycemic and hyperlipidemic effects of chlorpyrifos (CPF) after an acute exposure in rats. The mechanisms involved in hyperglycemia induced by CPF were studied. A single dose of CPF (50 mg kg⁻¹, subcutaneous, s.c.) was administered to overnight-fasted rats. Glucose and corticosterone levels, lipid status and paraoxonase (PON1) activity were determined in plasma of rats. Cardiovascular risk factors and the atherogenic index were calculated. Glycogen levels, tyrosine aminotransferase (TAT) and glucose-6-phosphatase (G6Pase) activities were determined in livers of rats. Cerebral acetylcholinesterase (AChE) activity was also determined. CPF caused an increase in glucose and glycogen levels as well as in TAT and G6Pase activities. The CPF exposure caused an increase in corticosterone levels, an inhibition of AChE activity and a reduction of PON1 activity. Regarding the lipid status, CPF induced an increase in triglycerides (TG) and low-density lipoprotein-cholesterol (LDL) levels and a decrease in high-density lipoprotein (HDL) levels associated with an increase of cardiovascular risk factors and the atherogenic index. The present study demonstrated that a single CPF administration caused hyperglycemia and hyperlipidemia in rats. The activation of the gluconeogenesis pathway, probably elicited by hypercorticosteronemia, is involved in the hyperglycemic effect of CPF in rats.     

Changes in lipid profiles of liver microsomes of rats following intratracheal administration of DDT or endosulfan

Abstract

The effect of intratracheal administration of DDT (5 mg/100 g body weight) or endosulfan (1 mg/100 g body weight) to rats for three consecutive days, has been studied on liver lipid metabolism. The administration of DDT but not endosulfan significantly increased the liver weight and the microsomal protein contents. Both DDT and endosulfan treatments significantly increased the contents of microsomal phosphatidylcholine (PC), total‐free‐ and esterified cholesterol. The distribution of unsaturated fatty acids of microsomal PC and PE was increased by DDT treatment. The intratracheal administration of DDT caused fatty infiltration of liver which was probably due to increased synthesis of triglycerides (TG). This is supported by the increased incorporation of radioactive palmitate‐l‐¹⁴C into microsomal TG. However, the increased incorporation of palmitate‐l‐¹⁴C into microsomal PC and phosphatidylethanolamine (PE) after the DDT treatment, was due to the increased transacylation reaction supported by the decreased activity of microsomal phospholipase A. The intratracheal adminstration of endosulfan did not has pronounced effect on liver fatty infiltration, or transacylation reaction in microsomal PC and PE. However, the results have shown that the treatments of DDT or endosulfan increased the PC contents and the incorporation of radioactive [methyl‐³H]choline into PC of microsomes, resulting the increased synthesis of PC via CDPcholine pathway. Thus, the intratracheally administered DDT or endosulfan to rats showed that both the insecticides cause manifestations in the biochemistry of microsomal membrane lipids, although the effects of DDT being more pronounced. Therefore, the translocation effects of these insecticides or metabolites from lung to liver is established.     

Metabolic and endocrine effects of bisphenol A exposure in market seller women with polycystic ovary syndrome

Bisphenol A (BPA) is one of the synthetic monomer which can be found in the environment. Limited animal and human studies have demonstrated that BPA alters endocrine and or metabolic functions. The aims of the present study were to evaluate serum BPA level in marketing seller women with polycystic ovary syndrome (PCOS) and hormonal and metabolic effects of this exposure compared to a control paired group. In a case-control study, 62 PCOS women who work as marketing sellers and 62 healthy women with similar jobs were included. The two groups were body mass index (BMI)- and age-matched. Serum samples were analyzed for BPA content, fasting blood sugar (FBS), triglyceride, cholesterol, HDL and LDL levels, thyroid stimulating hormone (TSH) concentration, and LH:FSH ratio. Significant higher serum BPA content (0.48 ± 0.08 vs. 0.16 ± 0.04 ng/ml), triglyceride (103.05 ± 13.10 vs. 91.65 ± 12.52 mg/dl), cholesterol (165.05 ± 10.79 vs. 161.21 ± 10.31 mg/dl) levels and LH:FSH ratio (3.64 ± 0.86 vs. 0.62 ± 0.14) and significant lower TSH concentration (1.56 ± 0.68 vs. 2.15 ± 1.09 IU/ml) were detected in case against control group, respectively (P < 0.05). No significant differences were detected in FBS, LDL, and HDL levels between the two groups. Also, there were no significant associations between serum TSH concentration and BPA level neither in case (P = 0.269) nor in control (P = 0.532) groups. In BPA-exposed PCOS women, BPA level was higher than healthy women and this difference maybe the cause of significant differences in levels of triglyceride, cholesterol, TSH, and LH:FSH ratio. These observations confirm the potential role of BPA in PCOS pathophysiology.     

Changes in lipid profiles of liver microsomes of rats following intratracheal administration of DDT or endosulfan

The effect of intratracheal administration of DDT (5 mg/100 g body weight) or endosulfan (1 mg/100 g body weight) to rats for three consecutive days, has been studied on liver lipid metabolism. The administration of DDT but not endosulfan significantly increased the liver weight and the microsomal protein contents. Both DDT and endosulfan treatments significantly increased the contents of microsomal phosphatidylcholine (PC), total-free- and esterified cholesterol. The distribution of unsaturated fatty acids of microsomal PC and PE was increased by DDT treatment. The intratracheal administration of DDT caused fatty infiltration of liver which was probably due to increased synthesis of triglycerides (TG). This is supported by the increased incorporation of radioactive palmitate-1-14C into microsomal TG. However, the increased incorporation of palmitate-1-14C into microsomal PC and phosphatidylethanolamine (PE) after the DDT treatment, was due to the increased transacylation reaction supported by the decreased activity of microsomal phospholipase A. The intratracheal administration of endosulfan did not have pronounced effect on liver fatty infiltration, or transacylation reaction in microsomal PC and PE. However, the results have shown that the treatments of DDT or endosulfan increased the PC contents and the incorporation of radioactive [methyl-3H]choline into PC of microsomes, resulting the increased synthesis of PC via CDPcholine pathway. Thus, the intratracheally administered DDT or endosulfan to rats showed that both the insecticides cause manifestations in the biochemistry of microsomal membrane lipids, although the effects of DDT being more pronounced. Therefore, the translocation effects of these insecticides or metabolites from lung to liver is established.     

The effect of malathion and gamma-BHC on the lipid metabolism in relation to reproduction in the tropical teleost, Clarias batrachus

In the present study, female Clarias batrachus were exposed to two sublethal concentrations of gamma-BHC (2 and 8 microg litre(-1)) and malathion (1 and 4 microl litre(-1)) for 4 weeks during different phases of their reproductive cycle. Impact of these pesticides on free fatty acids, monoglycerides, diglycerides, triglycerides, phospholipids, free and esterified cholesterol in the liver, plasma, ovary and muscle was assessed. During the pre-vitellogenic and regressed phases, they suppressed the levels of fatty acids and glycerides in the liver, but had no effect on their levels in the plasma, ovary and muscle. However, in the vitellogenic phase, fatty acids in the liver and plasma were increased, but were decreased in the ovary and muscle. Glycerides were also decreased in the studied tissues. In the post-vitellogenic phase, these pesticides increased the levels of fatty acids and glycerides in the liver and ovary, but decreased their levels in the plasma. Both pesticides decreased hepatic phospholipids in the pre-vitellogenic phase, while in the vitellogenic phase only gamma-BHC reduced its levels in the liver. These pesticides also restricted their mobilisation to the ovary. Cholesterol biosynthesis seemed unaffected, but the hydrolysis of esterified cholesterol to free cholesterol was adversely affected during the period of estrogen biosynthesis.     

Toxicological assessment of chlorinated diphenyl ethers in the rat, Part II

Chlorinated diphenyl ethers (CDE's) are environmental contaminants that have been found in Great Lakes fish. Because of the paucity of toxicity data and potential for human exposure, the present short-term study was conducted to assess their potential toxic effects. Groups of 10 male and 10 female rats were administered the three CDE congeners (2,2',4,4',5-pentachlorodiphenyl ether (PCDE), 2,2',4,4',5,5'-hexachlorodiphenyl ether (HCDE), 2,2',3,4,4',6,6'-heptachlorodiphenyl ether (HPCDE] in diets at levels of 0.5, 5.0, 50 or 500 ppm for a period of 4 weeks. Decreased food consumption was observed with male and female rats fed the diet containing 500 ppm HPCDE. Treatment with the three isomers at the highest dose level produced an increase in liver weight in both sexes. While administration of PCDE produced an increase in hepatic aminopyrine demethylase activity, HCDE caused a significant increase in aminopyrine demethylase, aniline hydroxylase and ethoxyresorufin de-ethylase activities. HPCDE caused a significant increase in ethoxyresorufin de-ethylase activity. HPCDE at the highest dose level also caused a significant reduction in circulating lymphocytes in male rats. The 3 CDE's produced mild and adaptative histological changes in the liver and thyroid, but only HPCDE elicited mild changes in the thymus, bone marrow, and spleen. The above data indicate that HPCDE is immunosuppressive and that all three CDE isomers are considered to be moderately toxic in rats. The no-observable effects levels appear to be between 5-50 ppm in diet (0.36-3.0 mg/kg b.w.) for the three CDE's.     

Effects of sodium arsenate exposure on liver fatty acid profiles and oxidative stress in rats

The present study aimed to evaluate the effect of arsenic on liver fatty acids (FA) composition, hepatotoxicity and oxidative status markers in rats. Male rats were randomly devised to six groups (n?=?10 per group) and exposed to sodium arsenate at a dose of 1 and 10 mg/l for 45 and 90 days. Arsenate exposure is associated with significant changes in the FA composition in liver. A significant increase of saturated fatty acids (SFA) in all treated groups (p?<?0.01) and trans unsaturated fatty acids (trans UFA) in rats exposed both for short term for 10 mg/l (p?<?0.05) and long term for 1 and 10 mg/l (p?<?0.001) was observed. However, the cis UFA were significantly decreased in these groups (p?<?0.05). A markedly increase of indicator in cell membrane viscosity expressed as SFA/UFA was reported in the treated groups (p?<?0.001). A significant increase in the level of malondialdehyde by 38.3 % after 90 days of exposure at 10 mg/l was observed. Compared to control rats, significant liver damage was observed at 10 mg/l of arsenate by increasing plasma marker enzymes after 90 days. It is through the histological investigations in hepatic tissues of exposed rats that these damage effects of arsenate were confirmed. The antioxidant perturbations were observed to be more important at groups treated by the high dose (p?<?0.05). An increase in the level of protein carbonyls was observed in all treated groups (p?<?0.05). The present study provides evidence for a direct effect of arsenite on FA composition disturbance causing an increase of SFA and TFAs isomers, liver dysfunction and oxidative stress. Therefore, arsenate can lead to hepatic damage and propensity towards liver cancer.     

Interactions of 2,2′,4,4′,5,5′-hexachlorobiphenyl and 2,3,7,8-tetrachlorodibenzo-p-dioxin in a subchronic feeding study in the rat

Female (SD) rats were fed diets containing 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and 2,2′,4,4′,5,5′-hexachlorobiphenyl (PCB 153) in various concentrations for three months. PCB 153 had no significant effect on the body weight gain when given alone or in combination with TCDD. The increases in relative liver weights were additive. For thymic atrophy no interactive effects became apparent. PCB 153 had no effect on the EROD induction by TCDD. PROD induction by PCB 153 was diminished in the presence of TCDD. The level of TCDD in the liver was decreased by PCB 153. Increasing TCDD dosage led to an increase in PCB 153 levels.     

Effects of honey HMF on enzyme activities and serum biochemical parameters of Wistar rats

Hydroxymethylfurfural (HMF) is a by-product of thermal degradation of glucose and fructose. In this study, the effects of high HMF content of honey on biochemical parameters of rats were investigated. Experiments were conducted with 40 Wistar albino male rats, each weighing 250–350 g and covered a period of 5 weeks. The animals were divided into five groups. The first group was served as control group. HMF was injected subcutaneously at a dose of 200 mg/kg rat b.w. to the animals in group 2. Group 3 was fed with honey that contains 10 mg HMF/kg honey. In group 4 and 5, there were honeys that contain significantly high HMF content due to long storage period (181 mg HMF/kg honey) and heat process (140 mg HMF/kg honey). At the end of the feeding process, biochemical blood parameters of rats were investigated. It was observed that there were no differences among the glucose, triglyceride, HDL cholesterol, uric acid, Na, GGT, and ALP parameters of the groups. On the other hand, significant differences were observed among the cholesterol, LDL, BUN, creatinine, Ca, P, Mg, K, Cl, total bilirubin, LDH, CPK, AST, ALT, total protein, and pseudocholinesterase values of the rats. The highest adverse effects were obtained from group HMF, and it was followed by groups SH (stored honey) and HH (heated honey). It can be concluded that high HMF content of honey may affect the human health adversely; thus, HMF in honey must be controlled by beekeepers.     

The effect of consumption of pork enriched by organic selenium on selenium status and lipid profile in blood serum of consumers

Abstract

The aim of the research was to evaluate the effect of consumption of selenium-enriched pork on selected health indicators of probands. The intake of feed mixture with increased organic selenium at the dose of 0.3?mg.kg^?1 probably increases selenium concentration in MSM (musculus semimembranosus). In the pork enriched with organic selenium, the concentration was higher by 1.045?±?0.10?mg.kg^?1 compared with the control group 0.701?±?0.05?mg.kg^?1 at significance P?<?0.001. Sixteen participants in the experiment were represented by 8 men at the average age of 41.5?±?11.9?years and 8 women at the average age of 41.4?±?7.9?years. All the probands consumed meat enriched with selenium three times a week during one month. By consumption of the enriched pork, there was an increase of the selenium concentration in blood serum of probands traced with selenium increase from 73.19?±?15.68?μg.L^?1 to 73.73?±?15.13?μg.L^?1 (P?>?0.05). From the results we can see that consumption of enriched pork with selenium was significantly manifested in lowering of total cholesterol levels, which was associated with LDL cholesterol lowering (P?<?0.05). Differences among the HDL cholesterol and triglycerides samples were not significant.     

Biochemical study on the protective role of folic acid in rabbits treated with chromium (VI)

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.     

Chronic exposure to contaminated drinking water stimulates PPAR expression in mice livers

Mice were fed with source water (SW) and tap water (TW) for 90 d to evaluate hepatotoxicity induced by the drinking water. Histopathologic observation showed no obvious damage to hepatic tissue in the SW and TW groups. However, microarray analysis indicated that the SW and TW exposures affected many metabolic pathways, among which PPAR (peroxisome proliferator-activated receptors) signaling was most susceptible. Immunohistochemical staining demonstrated that both PPAR-α and PPAR-γ were significantly increased in the exposure groups compared to control. Enzyme-linked immunosorbent assay revealed that PPAR-α expression level was increased from 23.37±0.53 ng g(-1) liver weight in control group to 26.60±1.43 ng g(-1) liver weight in SW group and 27.68±1.10 ng g(-1) liver weight in TW group (p<0.05). For PPAR-γ, the expression level was also significantly enhanced from 0.83±0.07 ng g(-1) liver weight in control group to 1.11±0.20 ng g(-1) liver weight in SW group and 1.16±0.07 ng g(-1) liver weight in TW group (p<0.05). The SW and DW posed no obvious hepatotoxicity on mice and PPAR-α/-γ could be used as a novel biomarker to assess public health risk induced by slightly contaminated drinking water.     

Tissue bioaccumulation patterns, xenobiotic biotransformation and steroid hormone levels in Atlantic salmon (Salmo salar) fed a diet containing perfluoroactane sulfonic or perfluorooctane carboxylic acids

In the present study, groups of juvenile Atlantic salmon (Salmo salar) were fed gelatine capsules containing fish-food spiked with PFOA or PFOS (0.2 mg kg⁻¹ fish) and solvent (methanol). The capsules were given at days 0, 3 and 6. Blood, liver and whole kidney samples were collected prior to exposure (no solvent control), and at days 2, 5, 8 and 14 after exposure (Note: that day 14 after exposure is equal to 7 d recovery period). We report on the differences in the tissue bioaccumulation patterns of PFOS and PFOA, in addition to tissue and compound differences in modulation pattern of biotransformation enzyme genes. We observed that the level of PFOS and PFOA increased in the blood, liver and kidney during the exposure period. Different PFOS and PFOA bioaccumulation patterns were observed in the kidney and liver during exposure- and after the recovery periods. Particularly, after the recovery period, PFOA levels in the kidney and liver tissues were almost at the control level. On the contrary, PFOS maintained an increase with tissue-specific differences, showing a higher bioaccumulation potential (also in the blood), compared with PFOA. While PFOS and PFOA produced an apparent time-dependent increase in kidney CYP3A, CYP1A1 and GST expression, similar effects were only temporary in the liver, significantly increasing at sampling day 2. PFOA and PFOS exposure resulted in significant decreases in plasma estrone, testosterone and cortisol levels at sampling day 2, and their effects differed with 17α-methyltestostrerone showing significant decrease by PFOA (also for cholesterol) and increase by PFOS. PFOA significantly increased estrone and testosterone, and no effects were observed for cortisol, 17α-methyltestosterone and cholesterol at sampling day 5. Overall, the changes in plasma steroid hormone levels parallel changes in CYP3A mRNA levels. Given that there are no known studies that have demonstrated such tissue differences in bioaccumulation patterns with associated differences in toxicological responses in any fish species or lower vertebrate, the present findings provide some potential insights and basis for a better understanding of the possible mechanisms of PFCs toxicity that need to be studied in more detail.     

Heavy metal uptake by two edible Amaranthus herbs grown on soils contaminated with lead, mercury, cadmium, and nickel

The uptake of an element by a plant is primarily dependent on the plant species, its inherent controls, and the soil quality. Amaranthus hybridus (green herbs) and Amaranthus dubius (red herbs) were chosen to investigate their response and ability to accumulate and tolerate varying levels of elements in their roots and shoots. Red herbs and green herbs were grown in soil pots contaminated with three mixtures of Cd(II), Ni(II), Pb(II), and Hg(II). Plants in the control treatment were grown in the absence of the heavy metals mixture. The distribution of Cd, Ni, Pb, and Hg in the plants (in roots, stems, and leaves) was determined in two stages. Stage 1, after 5 weeks of plant growth and stage 2, full grown after 10 weeks of growth. In the red herbs the Cd concentration in the leaves at stage 2 was 150 ppm and was present in higher concentrations than Ni, Hg, and Pb. At the highest contamination level, in the green herbs plant, Hg was present in the highest concentration in the root, i.e., 336 ppm at stage 1, while the level in the leaves was 7.12 ppm. Both the green and red herbs species showed an affinity for Ni and Cd with moderate to high levels detected in the leaves, respectively.     

Effect of cadmium on ATPase activities in rats fed on iron-deficient and sufficient diets

Male Sprague-Dawley rats were fed on different levels of cadmium mixed with purified diets containing iron or no iron for 8 weeks. The body weight gain, tissue weights, hemoglobin, hematocrit, liver and brain ATPase were measured at 2, 4 and 8 weeks after feeding. The hemoglobin and hematocrit values were the same in all rats fed on cadmium. The rats fed on iron-deficient diets mixed with cadmium showed a significant decrease in body weight gain. However, the rats receiving only the 100 ppm of cadmium in iron-sufficient diet showed a significant decrease in body weight gain. There were no significant changes in the weights of thymus, spleen, kidney, heart, brain and testes. However, the liver weights were decreased in the highest treatment of cadmium but the liver weight/body ratios were uneffected. Na+-K+ activated ATPase activity in brains of rats fed on cadmium were significantly decreased at 2, 4 and 8 weeks of treatment. The decrease was more pronounced in rats fed on iron-deficient diets. Oligomycin-sensitive (Mitochondrial) Mg2+ ATPase activity was also significantly decreased in liver and brain tissues of rats fed on cadmium. Oligomycin-insensitive Mg2+ ATPase activity, however, was not altered in any tissues tested. It appears that cadmium may be interfering with energy (ATP) production and utilization processes in rat brain and liver tissues.     

Low doses of chlorpyrifos interfere with spermatogenesis of rats through reduction of sex hormones

Use of pesticides results in indirect effects on human health. We aimed to evaluate implications of toxicological effects of subchronic chlorpyrifos exposure on reproductive function in male rats. A total of 48 adult Wistar male rats were separated into four groups (n = 12). Animals were gavaged with 2.5 mg/kg (T1), 5 mg/kg (T2), or 10 mg/kg (T3) body weight of chlorpyrifos (CPF) or distilled water (control) daily for 30 days. Organ weights, epididymal sperm parameters, DNA integrity, sex hormonal (FHS and LH) levels, and alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), and creatinine concentrations were determined on day 31. Another two sets of (four groups/set; n = 10) animals were orally treated with the same doses of CPF, control animal groups were treated with distilled water only for 30 days, and fertility indices and blood plasma acetylcholine esterase (AchE) were determined on day 31. Exposure to CPF resulted in a significant (p < 0.05) decrease in weights of testis and epididymis. An increase in liver weight resulted in reduced sperm counts and sperm motility and an increase in sperm abnormalities. Significant reduction in serum testosterone (p < 0.01), luteinizing hormone (p < 0.05), and follicular stimulating hormone (p < 0.05) levels was evident in animals treated with the highest dose. A significant decrease in the number of viable implantation sites and pups was observed in female rats mated with the T3 (p < 0.01) and T2 (p < 0.05) males. The ALT, AST, GGT, and creatinine contents were significantly increased (p < 0.05 and p < 0.01, respectively) on CPF exposure. A significant (p < 0.01) reduction in blood plasma AchE enzyme was observed with the highest dose. Our results demonstrated that prolonged exposure of CPF induces spermatogenesis damage, possibly through interference with sex hormones and AchE enzyme resulting in reduction of fertility. Therefore, awareness programs on handling CPF (pesticides) to enhance safety warrant minimization of its hazards.     

Role of alpha-tocopherol and beta-carotene in ameliorating the fenvalerate-induced changes in oxidative stress, hemato-biochemical parameters, and semen quality of male rats

Role of alpha-tocopherol (vitamin E), beta-carotene and/or their combination as antioxidants against the toxicity of fenvalerate on blood hematology, free radicals, biochemical parameters, and semen quality were studied in male rats. Fenvalerate (20 mg/kg BW), vitamin E (100 mg/kg BW), beta-carotene (10 mg/kg BW), and vitamin E plus beta-carotene (100 + 10 mg/kg BW, respectively) were given alone or in combination with fenvalerate. The tested doses were given to rats every other day for 30 days. Results obtained showed that fenvalerate significantly (P < 0.05) induced free radicals in plasma and brain and insignificantly in liver and testes. While, vitamin E, beta-carotene alone and/or in combination decreased the levels of free radicals in plasma, liver, testes, and brain. The activities of glutathione S-transferase (liver), alkaline phosphatase (plasma and liver), aspartate aminotransferase (plasma, liver, and testes) and alanine aminotransferase (plasma and liver) were significantly (P < 0.05) increased due to fenvalerate administration. The activity of acetylcholinesterase was significantly (P < 0.05) decreased in brain and plasma, while plasma glucose, urea, creatinine, and bilirubin concentrations were significantly (P < 0.05) increased in rats treated with fenvalerate. Also, results showed a significant (P < 0.05) alterations in plasma proteins, hematological parameters, body weight, and relative weights of organs. Sperm concentration and motility (%) were significantly (P < 0.05) decreased, while dead and abnormal sperm increased in rats exposed to fenvalerate. Vitamin E, beta-carotene alone and/or in combination did not cause any changes in the investigated parameters, but improved semen quality and minimized the toxic effect of fenvalerate. The obtained results demonstrated the beneficial influences of vitamin E, beta-carotene alone and/or in combination in reducing the harmful effects of fenvalerate.     

A simplified precise method for adjusting serum levels of persistent organohalogen pollutants to total serum lipids

In order to obtain biomarker values that reflect body burden of persistent organohalogen pollutants (POP), concentrations of lipophilic POP in serum or plasma are generally expressed on a lipid weight basis, and not on a fresh weight basis. There are two different approaches to determine the lipid content in serum and plasma. The gravimetric determination is more expensive, and longer experience is needed as compared with the preferable enzymatic determination. Clinical chemistry laboratories at most hospitals perform enzymatic determinations of cholesterol and triglycerides on a routine basis, whereas analysis of phospholipids is not part of these analyses. In the present study, therefore, we evaluated the association between the sum of measured triglyceride, cholesterol, and phospholipid levels in serum among 617 individuals with the sum of only triglyceride and cholesterol levels. There was a very strong linear association between the sums of serum concentrations of triglycerides and cholesterols and the total lipid concentrations. As much as 97.2% of the variation in total lipid concentrations was explained by the sum of the triglyceride and cholesterol concentrations, with the following regression: Total lipid=0.9+1.3 *(Cholesterol+Triglycerides). Almost identical relationships were recorded in subgroups with men, women and subjects of different age. Thus, total lipid concentrations in blood serum can be accurately estimated by analyzing only cholesterol and triglycerides in the matrix.     

Heavy Metal Uptake by Two Edible Amaranthus Herbs Grown on Soils Contaminated with Lead,Mercury, Cadmium,and Nickel

The uptake of an element by a plant is primarily dependent on the plant species, its inherent controls, and the soil quality. Amaranthus hybridus (green herbs) and Amaranthus dubius (red herbs) were chosen to investigate their response and ability to accumulate and tolerate varying levels of elements in their roots and shoots. Red herbs and green herbs were grown in soil pots contaminated with three mixtures of Cd(II), Ni(II), Pb(II), and Hg(II). Plants in the control treatment were grown in the absence of the heavy metals mixture. The distribution of Cd, Ni, Pb, and Hg in the plants (in roots, stems, and leaves) was determined in two stages. Stage 1, after 5 weeks of plant growth and stage 2, full grown after 10 weeks of growth. In the red herbs the Cd concentration in the leaves at stage 2 was 150 ppm and was present in higher concentrations than Ni, Hg, and Pb. At the highest contamination level, in the green herbs plant, Hg was present in the highest concentration in the root, i.e., 336 ppm at stage 1, while the level in the leaves was 7.12 ppm. Both the green and red herbs species showed an affinity for Ni and Cd with moderate to high levels detected in the leaves, respectively.     

The cardioprotective effects of L-carnitine on rat cardiac injury,apoptosis, and oxidative stress caused by amethopterin

Amethopterin is used as a chemotherapeutic agent, and its antioxidant activity is used to treat many cancer types. This study aimed to study the ameliorating effect of L-carnitine against amethopterin-induced cardiac injury and oxidative stress in male rats. Sixty male albino rats were equally divided into six groups; the first and second groups were the control and L-carnitine groups, respectively, while the third group was treated with amethopterin rat group; the fourth and fifth groups were co-treated and post-treated with amethopterin rat with L-carnitine, respectively, and the sixth group was self-treated with amethopterin rat group. Cholesterol, triglycerides, low-density lipoprotein (LDL), glutathione, and total protein levels in amethopterin group showed a significant decrease when compared with control group, while high-density lipoprotein (HDL), glutamic oxaloacetic transaminase (GOT), malondialdehyde (MDA), catalase, and nitric oxide (NO) levels in amethopterin group showed a significant increase when compared with control group. Cholesterol, triglycerides, LDL, GOT, MDA, and catalase levels in the self-treated group showed a significant increase when compared with amethopterin group, while glutathione, total protein, and NO levels in the self-treated group showed significant decrease when compared with amethopterin group. Many of abnormalities as moderate hydrophobic changes of myofibrillar structure with striations, myocardial atrophy, cytoplasmic vacuoles, edema, and leukocyte infiltration were detected in cardiac tissues in amethopterin rat group. A significant increase of the apoptotic protein p53 and CD68 immunoreactivity, despite a significant decrease in the antiapoptotic Bcl–2 proteins after amethopterin injection when compared with control group, was observed. Treatment (co and post) with L-carnitine improved the biochemical, histopathological, and immunohistochemical alterations in the heart treated with amethopterin.