Green synthesized silver nanoparticles for the treatment of diabetes and the related complications of hyperlipidemia and oxidative stress in diabetic rats.

This study was conducted to compare the impact of cinnamon silver nanoparticles (C-Ag-NPs) and cinnamon aqueous extract (CAE) on the total body weight (TBW), body weight gain (BWG), blood count (BC), fasting blood glucose (FBG), triglycerides (TGs), total cholesterol (TC), low-density (LDL-C) and high-density (HDL-C) lipoprotein cholesterol, liver function enzymes, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) of normal and streptozotocin (STZ) diabetic rats. The CAE was administered to rats at different doses (50.0 and 100.0 mg/kg bw), whereas the C-Ag-NPs were ingested at doses of 25.0 and 50.0 mg/kg bw for 30 days. At the end of the experiment, the administration of high or low dosages of CAE or C-Ag-NPs to diabetic rats significantly reduced the FBG, TC, TG, and LDL-C and significantly increased the HDL-C compared with the diabetic control rats. The highest dose (50.0 mg/kg bw) of the C-Ag-NPs was the most efficient at significantly reducing (P < 0.05) the levels of all the analyzed parameters compared with the CAE. However, the treated and normal rats did not show any hypoglycemic activity after ingesting the CAE or C-Ag-NPs. Such effects were associated with considerable increases in their BWG. The diabetic rats that ingested the CAE or C-Ag-NPs showed a gradual decrease in their FBG, TC, LDL, and TG levels, but they were still higher than those in the normal rats. Furthermore, the C-Ag-NPs and CAE considerably enhanced the hepatic (GPT, GOT, ALP, and GGT) and antioxidant biomarker enzyme activities (SOD, CAT, and GPx) in diabetic rats. Relative to the untreated diabetic control, the C-Ag-NPs were more effective than the CAE in the diabetic rats. The C-Ag-NPs exhibited a protective role against hyperglycemia and hyperlipidemia in the diabetic rats and modulated their liver function enzyme biomarkers and antioxidant enzyme activities more than the CAE.

Evaluation of Nano-curcumin effects against Tartrazine-induced abnormalities in liver and kidney histology and other biochemical parameters.

In the current study, 40 albino male rats were investigated to evaluate the impact of Nano-curcumin (Nano-CUR) administration against Tartrazine (TZ)-induced variations in kidney and liver histology and their related functions. The liver function biomarkers are (glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transaminase (GGT), alkaline phosphatase (ALP), total bilirubin (T. BiLL)), whereas the kidney biomarkers are (creatinine, uric acid, urea, globulin, total protein (TP)), as well as blood parameters of (serum glucose (sGlu), alpha-fetoprotein (AFP), protein Kinase-C (PKC)) and lipid profiles that include (total lipids (TL), triglyceride (TG), total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), high-density L-C (HDL-C), and very-low-density L-C (VLDL-C)). The collected rats were randomly separated into four different groups (G1, G2, G3, and G4) of 10 rats each, where G1 stands for control, G2 for TZ-ingestion, G3 for Nano-CUR-ingestion, and G4 for (TZ + Nano-CUR mix.) ingestion. TZ-ingestion significantly (p < .05) increases the liver function enzymes' activity, total bilirubin and kidney biomarkers (creatinine, urea, uric acid, total protein (TP), globulin (Glu)). Also, TZ-ingestion significantly increased sGlu, PKC, AFP, as well as lipid profiles, while there were significant (p < .05) decreases in HDL-C and albumin (Alb) concentrations compared to control. Histopathological changes in liver, such as dilatation of blood sinusoids and central vein with hemorrhage and necrosis, were observed due to TZ-ingestion. Similarly, TZ-ingestion influenced kidney tissues in terms of tubular dilatation with tubular degeneration, thickened basement membrane, and dilatation of the glomerular capillaries. Markedly, the administration of Nano-CUR significantly decreased liver and kidney function enzymes as well as sGlu, AFP, and PKC, whereas it significantly increased serum Alb and HDL-C levels compared to control and TZ-ingested rats. All values arranged around normal control values. Also, the liver tissue of Nano-CUR-ingested rats showed a normal arrangement of normal blood sinusoids(s), hepatic cords, and hepatocytes as compared to controls. The same results were also found in the section of rat kidney ingested with 2.00 g of Nano-CUR/(kg B.W.) showing near-normal architecture as compared to control rats. The liver tissue of rats ingested by a mixture of (7.5 mg of TZ + 2.0 g of Nano-CUR/kg B.W.) showed little necrosis. Similarly, a section of rat kidney ingested a mixture of (7.5 mg of TZ + 2.00 g of Nano-CUR/kg B.W.) which revealed mild tubular degeneration and dilatation of the glomerular capillaries. These results support the protective and therapeutic effects of Nano-CUR on the histology of liver and kidneys and their related function biomarkers. Also, Nano-CUR corrects the imbalance in serum glucose (sGlu), AFP, PKC, and lipid profiles in TZ-ingested rats compared to control.

Regulatory Role of Nano-Curcumin against Tartrazine-Induced Oxidative Stress, Apoptosis-Related Genes Expression, and Genotoxicity in Rats.

The present study evaluates the regulatory effect of Nano-Curcumin (Nano-CUR) against tartrazine (TZ)-induced injuries on apoptosis-related gene expression (i.e., p53, CASP-3 and CASP-9), antioxidant status, and DNA damages in bone marrow in treated rats. Male rats were arbitrarily separated into five groups, and each group was comprised of 10 rats each. The 1st group served as control (G1). The 2nd group ingested 7.5 mg TZ/kg. b.w. (body weight). The 3rd group ingested Nano-CUR 1 g/kg b.w. The 4th and 5th groups were respectively administered with (1 g Nano-CUR + 7.5 mg TZ/kg. b.w.) and (2 g Nano-CUR + 7.5 mg TZ/kg. b.w.). At the end of the experiment, blood samples, livers, and kidneys were collected. Livers and kidneys were homogenized and used for the analysis of reduced glutathione, malonaldhyde, total antioxidant capacity, lipid peroxide antioxidant enzyme activities, apoptosis-related gene expression, and genotoxicity by comit test. The ingestion of TZ for 50 days resulted in significant decreases in body, and kidney weights in rats and a relative increase in the liver weight compared to control. In contrast, the ingestion of Nano-CUR with TZ remarkably upgraded the body weight and relative liver weight compared to the normal range in the control. Aditionally, TZ ingestion in rats increased the oxidative stress biomarkers lipid peroxide (LPO) and malonaldehyde (MDA) significantly, whereas it decreased the reduced glutathione (GSH) levels and total antioxidant capacity (TAC). Similarly, the levels of glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) significantly deteriorated in response to TZ ingestion. Moreover, the results revealed a remarkable up-regulation in the level of expression for the three examined genes, including p53, CASP-3, and CASP-9 in TZ-ingested rats compared to the control. On the other hand, the comet assay result indicates that the ingestion of TZ induced DNA damage in bone marrow. Notably, the administration of Nano-CUR protected the kidney and liver of TZ-ingested rats as evidenced by a significant elevation in all antioxidant activities of tested enzymes (i.e, SOD, GPx, and CAT), vital recovery in GSH and TAC levels, and a statistical decrease in LPO and MDA compared to TZ-ingested rats. Interestingly, the ingestion of rats with TZ modulates the observed up-regulation in the level of expression for the chosen genes, indicating the interfering role in the signaling transduction process of TZ-mediated poisoning. The results indicate that the administration of Nano-CUR may protect against TZ-induced DNA damage in bone marrow. According to the results, Nano-CUR exerted a potential protective effect against oxidative stress, DNA damage, and the up-regulation of apoptosis-related genes induced by TZ ingested to rats.

Seasonal concentrations of lead in outdoor and indoor dust and blood of children in Riyadh, Saudi Arabia.

Because detrimental effects of exposure to lead (Pb) on human health have been observed, we previously investigated concentrations of Pb in water supplies and blood of adult residents of Riyadh, Saudi Arabia. The objectives of the present study were to: (1) examine seasonal rates of deposition of Pb in dust in several areas of Riyadh city, (2) measure concentrations of Pb in both outdoor and indoor dust, (3) compare concentrations of Pb in dust in Riyadh with those reported for other cities, and (4) quantify Pb in blood of children living in Riyadh. Mean, monthly deposition of PB in outdoor dust was 4.7 × 10(1) ± 3.6 tons km(-2), with a mean Pb concentration of 2.4 × 10(2) ± 4.4 × 10(1) µg/g. Mean, monthly deposition of Pb in indoor dust was 2.7 ± 0.70 tons km(-2), with a mean concentration of 2.9 × 10(1) ± 1.5 × 10(1) µg Pb/g. There was a significant (P < 0.01) correlation between concentrations of Pb in outdoor and indoor dust. There was no correlation between concentrations of Pb in indoor dust and that in blood of children of Riyadh, whereas there was a weakly significant (P < 0.05) correlation between concentrations of Pb in outdoor dust and that in blood of children. The mean (±SD) concentration of Pb in blood of children in Riyadh was 5.2 ± 1.7, with a range of 1.7-1.6 × 10(1) µg/dl. Concentrations of Pb in blood of 17.8 % of children in Riyadh were greater than 10 µg/dl, which is the CDC's level of concern.

Improvement of mercuric chloride-induced testis injuries and sperm quality deteriorations by Spirulina platensis in rats.

The present study was undertaken to investigate the protective effect of the filamentous cyanobacterium Spirulina platensis (S. platensis) on mercury (II) chloride (HgCl(2))-induced oxidative damages and histopathological alterations in the testis of Wistar albino rats. The animals were divided into four equal groups, i) control, ii) HgCl(2), iii) S. platensis and iv) combination of HgCl(2)+S. platensis. Oxidative stress, induced by a single dose of HgCl(2) (5 mg/kg, bw; subcutaneously, s.c.), substantially decreased (P<0.01) the activity level of testicular key enzymatic antioxidant biomarkers (superoxide dismutase, SOD; catalase, CAT and glutathione peroxidase, GPx), oxidative stress makers (blood hydroperoxide; testicular reduced glutathione, GSH and malondialdehyde, MDA), and testicular mercury levels. Moreover, HgCl(2) administration resulted in a significant (P<0.01) increase in the number of sperms with abnormal morphology and decrease in epididymal sperm count, motility, plasma testosterone level and testicular cholesterol. Furthermore, HgCl(2) exposure induced histopathological changes to the testis including morphological alterations of the seminiferous tubules, and degeneration and dissociation of spermatogenic cells. Notably, oral pretreatment of animals with Spirulina (300 mg/kg, bw) lowered the extent of the observed HgCl(2)-mediated toxicity, whereby significantly reducing the resulting lipid peroxidation products, mercury accumulation in the testis, histopathological changes of the testes and spermatozoal abnormalities. In parallel, the pretreatment with Spirulina also completely reverted the observed Hg-Cl(2)-induced inhibition in enzymatic activities of antioxidant biomarkers (SOD, CAT and GPx) back to control levels. The pretreatment of rats with S. platensis significantly recovered the observed HgCl(2)-mediated decrease in the weight of accessory sex organs. Taken together, our findings clearly highlight the role of S. platensis as a protective modulator of HgCl(2)-induced testicular injuries and suggest some therapeutic potential in mammals. Further investigation of therapeutic strategies employing Spirulina against heavy metals toxicity in humans is therefore warranted.

Daily intake of selenium and concentrations in blood of residents of Riyadh City, Saudi Arabia.

Concentrations of selenium (Se) in food from local markets of Riyadh, Kingdom of Saudi Arabia (KSA) were measured and daily intake calculated based on information from a questionnaire of foods eaten by healthy Saudis. The daily intake of Se was then compared to concentrations of Se in blood serum. Primary sources of Se in the diet of Saudis were as follows: meat and meat products (31%), egg (20.4%), cereals and cereal products (16%), legumes (8.7%), fruits (6.8%), milk and dairy products (2.0%), beverages (2%), sweets (1.8%), pickles (0.2%), and oil (0.02%). Daily intake of Se, estimated to be 93 µg Se/person/day, was slightly greater than that calculated from the Food and Agriculture Organization (FAO) food balance sheet for KSA, which was approximately 90 µg Se/person/day. The daily intake of Se by Saudis in Riyadh was greater than that of Australians or Dutch but less that of Canadians and Americans. There was a statistically significant correlation (R = +0.38, P < 0.05) between daily intake of Se and concentrations of Se in blood serum of Saudis in Riyadh. The mean concentration of Se in serum was 1.0 × 10(2) ± 30.5 µg Se/l. Taken together, the results suggest that the average Se intake and Se serum concentrations are within the known limits and recommendations, making it unlikely that Saudis are on average at risk of deficiency or toxicity.

Hepatoprotective effects of vitamin E/selenium against malathion-induced injuries on the antioxidant status and apoptosis-related gene expression in rats.

The present study is undertaken to evaluate the protective effect of vitamin E (α-tocopherol) and selenium (Se) against malathion (MTN)-induced oxidative stress and hepatic injuries in experimental rats. Male rats were randomly divided into eight groups comprised of 10 rats each. The 1(st) group served as a negative control (C(N)), whereas the 2(nd) was supplemented with a combination of α-tocopherol (100 mg kg(-1) body weight, b.w.)/Se (0.1 mg kg(-1) bw). The 3(rd), 4(th) and 5(th) groups were respectively administered with increasing doses of MTN equivalent to (1/50 )LD(50) (M(1/50)), (1/25) LD(50) (M(1/25)) and (1/10) LD(50) (M(1/10)), respectively. The 6(th), 7(th) and 8(th) groups were administered the same doses of MTN as in the 3(rd), 4(th) and 5(th) groups with a concomitant supplementation with α-tocopherol/Se. Subchronic exposure of rats to MTN for 45 days resulted in statistical dose-dependent decrease in acetylcholinestrase (AChE) activity, increase in oxidative stress marker lipid peroxidation (LPO) and reduction in reduced glutathione (GSH) level. Moreover, the levels of glutathione persoxidase (GPx), superoxide dismutase (SOD) and catalase (CAT) were significantly decline in response to MTN exposure in a dose-dependent fashion. Furthermore, histopathological studies of liver in the rats which received MTN exhibited, moderate to severe degenerative and necrotic changes in the hepatocytes. Notably, the administration of α-tocopherol/Se protected the liver of rats exposed to MTN as evidenced by the appearance of normal histological structures, significant attenuation of the decline in all antioxidant enzymes tested (i.e. GPx, SOD and CAT), significant recovery in the GSH level and statistical reduction in LPO, as compared to the experimental rat. The effect of α-tocopherol/Se supplementation on transcriptional activity of three key stress and apoptosis-related genes (i.e., Tp53, CASP3 and CASP9), in response to MTN exposure in rats, was investigated. Results revealed a significant concentration-dependent up-regulation in the level of expression for the three genes examined, in response to MTN exposure, compared with the control. Interestingly, the supplementation of MTN-treated rats with α-tocopherol/Se modulates the observed significant dose-dependent up-regulation in the level of expression for three selected genes, indicative of an interfering role in the signaling transduction process of MTN-mediated poisoning. Taken together, these data suggest that the administration of α-tocopherol/Se may partially protect against MTN-induced hepatic oxidative stress and injuries.