Deltamethrin and Its Nanoformulations Induce Behavioral Alteration and Toxicity in Rat Brain through Oxidative Stress and JAK2/STAT3 Signaling Pathway.

Deltamethrin (DM) is the most powerful synthetic pyrethroid that has toxicity to the central nervous system and results in behavioral changes in both animals and humans. This effect is mediated by inducing alterations in the action of neurotransmitters and brain pathological changes. Nanocarrier encapsulated pesticides may decrease the toxicity of pesticides. Thus, this study aimed to determine the effect of an inorganic metal carrier (silica Nps) and polymeric capsule (chitosan Nps) of deltamethrin nano-formulations on antioxidant levels and oxidative stress in the brain and on behavior of the male albino rat. Sixty male albino rats were equally divided into four groups. Group I: control group; group II given DM liquefied in corn oil at 3.855 mg/kg BW; group III receiving silica-loaded deltamethrin (S/DM Nps) at 8.795 mg/kg BW; and group IV: given chitosan encapsulated deltamethrin (CS/DM Nps) at 30.44 mg/kg BW. All treatments were given orally for four weeks. Following this, behavioral tests were conducted to record locomotor activity, anxiety like behaviors, exploration, and the short memory of rats. In addition, brain antioxidant/oxidant, serum neurotransmitters such as acetylcholine esterase (AchE) and monoamine oxidase (MAO), JAK2 and STAT3 gene and proteins expression were measured. The DM group showed a highly significant elevation in malondialdehyde content, MAO, AchE, vascular endothelial growth factor (VEGF) levels, and the expression level of neurogenic genes, JAK2 and STAT3, in comparison with the control group. Both S/DM Nps and CS/DM Nps significantly decreased MAO, AchE, and VEGF compared with the DM group. Moreover, both S/DM Nps and CS/DM Nps significantly decreased the gene and proteins expression of JAK2 and STAT3 compared with the DM group. These alterations were evidenced by the deficiency in memory and learning behaviors that were accompanied by histopathological findings of the hippocampus and the cortex. It was concluded that the nano formulations containing DM induced less neurobehavioral toxicity than free DM. Additionally, the use of nanocarriers reduced the damage to health and the environment.

Naringin and Hesperidin Counteract Diclofenac-Induced Hepatotoxicity in Male Wistar Rats via Their Antioxidant, Anti-Inflammatory, and Antiapoptotic Activities.

This study is aimed at evaluating the preventive effect and at suggesting the mode of actions of naringin and hesperidin and their combination in diclofenac-induced hepatotoxicity. Male Wistar rats, intraperitoneally injected with diclofenac sodium (3 mg/kg b.wt/day), were orally treated with naringin (20 mg/kg b.wt/day) and hesperidin (20 mg/kg b.wt/day) and their combination for 4 weeks. The administrations of naringin and hesperidin to diclofenac-injected rats led to a significant decrease in the elevated serum ALT, AST, LDH, ALP, GGT, total bilirubin, TNF-α, and IL-17 levels as well as liver lipid peroxidation and liver p53 and caspase-3 mRNA expressions. In contrast, serum IL-4 level, liver GSH content, and liver GPx and SOD activities increased. In association, diclofenac-induced deleterious histological alterations including hydropic degeneration, cytoplasmic vacuolization, apoptosis, and focal hepatic necrosis of hepatocytes associated with inflammatory cells' infiltration were remarkably improved by treatments with naringin and hesperidin. In conclusion, naringin, hesperidin, and their combination, which was the most potent, counteract diclofenac-induced liver injury via antioxidant, anti-inflammatory, and antiapoptotic actions. Thus, this study recommends the use of naringin and hesperidin or their combination to resolve the side effects of drugs like diclofenac on the liver.

Therapeutic effect of mesenchymal stem cells on histopathological, immunohistochemical, and molecular analysis in second-grade burn model.

BACKGROUND AND AIM: Deleterious cutaneous tissue damages could result from exposure to thermal trauma, which could be ameliorated structurally and functionally through therapy via the most multipotent progenitor bone marrow mesenchymal stem cells (BM-MSCs). This study aimed to induce burns and examine the effect of BM-MSCs during a short and long period of therapy. MATERIAL AND METHODS: Ninety albino rats were divided into three groups: group I (control); group II (burn model), the animals were exposed to the preheated aluminum bar at 100°C for 15 s; and group III (the burned animals subcutaneously injected with BM-MSCs (2×106 cells/ ml)); they were clinically observed and sacrificed at different short and long time intervals, and skin samples were collected for histopathological and immunohistochemical examination and analysis of different wound healing mediators via quantitative polymerase chain reaction (qPCR). RESULTS: Subcutaneous injection of BM-MSCs resulted in the decrease of the wound contraction rate; the wound having a pinpoint appearance and regular arrangement of the epidermal layer with thin stratum corneum; decrease in the area percentages of ADAMs10 expression; significant downregulation of transforming growth factor-ß (TGF-ß), interleukin-6 (IL-6), tumor necrotic factor-α (TNF-α), metalloproteinase-9 (MMP-9), and microRNA-21; and marked upregulation of heat shock protein-90α (HSP-90α) especially in late stages. CONCLUSION: BM-MSCs exhibited a powerful healing property through regulating the mediators of wound healing and restoring the normal skin structures, reducing the scar formation and the wound size.

Musa paradisiaca L. leaf and fruit peel hydroethanolic extracts improved the lipid profile, glycemic index and oxidative stress in nicotinamide/streptozotocin-induced diabetic rats.

This study aimed to assess antihyperlipidemic, cardiac and antioxidant effects as well as mode of actions of Musa paradisiaca (M. paradisiaca) leaf and fruit peel hydroethanolic extracts in nicotinamide (NA)/streptozotocin (STZ)-induced diabetic rats. Experimental diabetes mellitus was induced by a single intraperitoneal injection of STZ (60 mg/kg body weight), 15 min after intraperitoneal injection of NA (120 mg/kg body weight). NA/STZ-induced diabetic rats were orally supplemented with M. paradisiaca leaf and fruit peel hydroethanolic extracts in a dose of 100 mg/kg body weight/day for 28 days. The treatment of NA/STZ-induced diabetic rats with M. paradisiaca leaf and fruit peel extracts significantly decreased the elevated fasting and post-prandial serum glucose, total cholesterol, triglycerides, LDL-cholesterol and vLDL-cholesterol levels and significantly increased the lowered serum insulin level, liver glycogen content, serum HDL-cholesterol level, homeostasis model assessment-insulin resistance (HOMA-IS) and HOMA-ß cell function. The elevated cardiovascular risk indices in diabetic rats were significantly improved due to treatment with M. paradisiaca extracts. Concomitant with the increase in liver glycogen content, the glucose-6-phosphatase activity significantly decreased reflecting the decrease in hepatic glucose output. The heart function was potentially ameliorated as manifested by decrease in the elevated serum creatine kinase-MB, lactate dehydrogenase and aspartate aminotransferase activities after treatments of diabetic rats with M. paradisiaca extracts. The elevated liver lipid peroxidation and the decline in liver glutathione content and superoxide dismutase, glutathione peroxidase and glutathione-S-transferase activities were significantly reversed by treatments. Thus, it can be concluded that M. paradisiaca leaf and fruit peel hydroethanolic extracts may have antihyperlipidemic and cardioprotective potentials in NA/STZ-induced diabetic rats. These effects may be mediated via improvements in the glycemic state, ß-cell function, tissue insulin sensitivity, and antioxidant defense mechanism.

Corrigendum to "Dietary Lipids in Health and Disease".

[This corrects the article DOI: 10.1155/2019/5729498.].

Antihyperglycemic Effects and Mode of Actions of Musa paradisiaca Leaf and Fruit Peel Hydroethanolic Extracts in Nicotinamide/Streptozotocin-Induced Diabetic Rats.

The present study aimed to evaluate the antihyperglycemic effects of Musa paradisiaca (M. paradisiaca) leaf and fruit peel hydroethanolic extracts and to suggest their probable mode of actions in nicotinamide (NA)/streptozotocin (STZ)-induced diabetic rats. The leaf and fruit peel hydroethanolic extracts were analyzed by GC-MS that indicated the presence of phytol, octadecatrienoic acid, hexadecanoic acid, and octadecadienoic acid as major components in the leaf extract and vitamin E, octadecenamide, ß-sitosterol, and stigmasterol as major phytochemicals in the fruit peel extract. Diabetes mellitus was induced by a single intraperitoneal injection of STZ (60 mg/kg body weight) dissolved in citrate buffer (pH 4.5), 15 minutes after intraperitoneal injection of NA (120 mg/kg body weight). The NA/STZ-induced diabetic rats were, respectively, treated with M. paradisiaca leaf and fruit peel hydroethanolic extracts at a dose of 100 mg/kg body weight/day by oral administration for 28 days. The treatment of NA/STZ-induced diabetic rats with leaf and fruit peel extracts significantly improved the impaired oral glucose tolerance and significantly increased the lowered serum insulin and C-peptide levels. The HOMA-IR (as the index of insulin resistance) and QUICKI (as a marker for insulin sensitivity), as well as HOMA-ß cell function were significantly alleviated as a result of treatment of diabetic rats with leaf and fruit peel extracts. In association, the elevated serum-free fatty acids, TNF-α, and IL-6 levels were significantly decreased. In addition, the suppressed adipose tissue PPARγ, GLUT4, adiponectin, and insulin receptor ß-subunit mRNA expressions were upregulated while the elevated adipose tissue resistin expression was downregulated in diabetic rats as a result of treatment with the leaf and peel extract. Based on these results, it can be concluded that M. paradisiaca leaf and fruit peel hydroethanolic extracts have antihyperglycemic effects which may be mediated via their insulinotropic and insulin-sensitizing effects.

Modeling of the irradiation effect on some physicochemical properties of metoprolol tartrate for safe medical uses.

The effect of gamma-irradiation and ionizing radiation (high-energy electrons beam) on the physicochemical properties of metoprolol tartrate at the solid phase and aqueous solution, has been investigated in the present study to model some properties affected by absorbed doses and to reveal some interesting mutual causal correlation. The proposed some interesting models can be adapted to other experimental conditions, and the newly obtained values of the adjustable parameters could be an excellent criterion of the state quality of the metoprolol tartrate or for other additional interpretations. The peculiar behaviour of variation of physicochemical properties against dose leads us to confirm the suggested optimized doses mentioned in previous work, for sterilization and safe medical uses.

Antenatal care utilisation among Syrian refugees in Tehran: A respondent driven sampling method.

AIM: To assess the antenatal care utilisation among Syrian refugees in Tehran. METHODS: This cross-sectional study was performed in 2016 in Tehran. As the refugees live in the city, we used Respondent Driven Sampling method for finding participants. Data were collected from interviews by a newly graduated Syrian general practitioner. FINDINGS: In total, 231 women participated in the study. The mean (standard deviation) number of antenatal care visits was 3.73 (1.41) and 131(56.7%) women received at least four visits. The mean (standard deviation) number of antenatal care visits was higher among women with four or more living children compared with those with four or more: 3.47 (1.35); 95% confidence interval 3.28 to 3.66 vs. 2.82 (1.64); 95% confidence interval 2.25 to 3.40, p=0.01. The mean (standard deviation) number of antenatal care visits was higher among women whose spouses had academic degrees compared with those with lower education: 4.13 (1.37); 95% confidence interval 3.86-4.40 vs. 3.28 (1.31); 95% confidence interval 3.05-3.52, p<0.001. CONCLUSIONS: Antenatal care utilisation of Syrian women in Tehran complied with neither national guidelines of Iran nor the recommendations of World Health Organization. However, antenatal care utilisation of Syrian women in Tehran was higher than the main destinations of Syrian refugees. Syrian women kept their own cultural behaviour in terms of antenatal care utilisation.

The Preventive Effects and the Mechanisms of Action of Navel Orange Peel Hydroethanolic Extract, Naringin, and Naringenin in N-Acetyl-p-aminophenol-Induced Liver Injury in Wistar Rats.

N-Acetyl-p-aminophenol (APAP) or acetaminophen is the most common drug ingredient worldwide. It is found in more than 600 different over-the-counter and prescription medicines. Its long-term and overdose use is highly toxic and may result in liver injury. Thus, this study was designed to assess the preventive effects and to suggest the mechanisms of action of the navel orange peel hydroethanolic extract, naringin, and naringenin in APAP-induced hepatotoxicity in male Wistar rats. APAP was administered to male Wistar rats at a dose level of 0.5 g/kg body weight (b.w.) by oral gavage every other day for 4 weeks. APAP-administered rats were treated with the navel orange peel hydroethanolic extract (50 mg/kg b.w.), naringin (20 mg/kg b.w.), and naringenin (20 mg/kg b.w.) by oral gavage every other day during the same period of APAP administration. The treatments of APAP-administered rats with the peel extract, naringin, and naringenin produced a significant decrease in the elevated serum AST, ALT, ALP, LDH, and GGT activities as well as total bilirubin and TNF-α levels while they induced a significant increase in the lowered serum albumin and IL-4 levels. The treatments also resulted in a significant decrease in the elevated liver lipid peroxidation and enhanced the liver GSH content and SOD, GST, and GPx activities as compared with APAP-administered control; the peel extract was the most potent in improving the liver LPO, GSH content, and GPx activity. In addition, the three treatments significantly downregulated the elevated hepatic proapoptotic mediators p53, Bax, and caspase-3 and significantly upregulated the suppressed antiapoptotic protein, Bcl-2, in APAP-administered rats. In association, the treatments markedly amended the APAP-induced liver histopathological deteriorations that include hepatocyte steatosis, cytoplasmic vacuolization, hydropic degeneration, and necrosis together with mononuclear leucocytic and fibroblastic inflammatory cells' infiltration. In conclusion, the navel orange peel hydroethanolic extract, naringin, and naringenin may exert their hepatopreventive effects in APAP-administered rats via enhancement of the antioxidant defense system and suppression of inflammation and apoptosis.

Thiazolidinedione induces a therapeutic effect on hepatosteatosis by regulating stearoyl-CoA desaturase-1, lipase activity, leptin and resistin.

Hepatosteatosis is a disease present worldwide, which presents a number of health problems. Recently, thiazolidinedione (TZD) has been used as a therapy for lipid disorders. The present study demonstrates the potential of TZD as a treatment for hepatosteatosis and its mechanism of action, particularly focusing on its role in lipid metabolism. A total of 60 (80-90 g) rats were divided into three groups: A normal group with a standard diet, a high-fat, high-carbohydrate diet (HFCD) group or a HFCD+TZD group (n=20/group). The HFCD induced hepatosteatosis over a period of 12 weeks and the HFCD+TZD group were administered TZD in weeks 13-16. Blood and tissue samples were collected to measure hepatic function, the lipid profile, metabolism and hormone biomarkers, including serum triglyceride (TG), lipoprotein lipase (LPL), stearoyl-CoA desaturase (SCD-1), leptin and resistin. The HFCD-fed rats exhibited a significant increase in serum TG, total cholesterol, low-density lipoproteins, alanine transaminase and bilirubin compared with the normal group as well as a significant decrease in high-density lipoprotein. In addition, serum leptin and resistin were significantly elevated in the HFCD group compared with the normal group. The administration of TZD significantly increased SCD-1 activity and significantly inhibited LPL activity. It also attenuated the changes in the lipid profiles and normalized serum leptin and resistin levels. The results of the present study indicated that HFCD induced lipid abnormalities associated with hypertriglyceridemia, hypercholesterolemia and hepatosteatosis. These changes resulted from disruption to leptin and resistin, which may be due to alterations in LPL and SCD-1 activity. TZD mitigated the effects of HFCD-induced hepatosteatosis, indicating a possible regulatory effect of TZD in the development of hepatosteatosis. The authors suggest that the manipulation of SCD-1 and lipase by TZD may be useful as a treatment for hepatosteatosis.

Efficacy of functional foods mixture in improving hypercholesterolemia, inflammatory and endothelial dysfunction biomarkers-induced by high cholesterol diet.

BACKGROUND: Hypercholesterolemia associated with cardiovascular diseases is a global health issue that could be alleviated by functional foods. This study aimed to explore the effects of a high-cholesterol diet on lipid profile, cardiac, inflammatory, and endothelial dysfunction biomarkers, and the possible improvement by functional foods mixture. METHODS: Male albino rats weighing 100-150 g were randomly divided into four equal groups: 1st control, giving a normal diet; the 2nd received high-cholesterol diet for 8 weeks, the 3rd received the high-cholesterol diet + functional foods mixture, and the 4th administered high-cholesterol diet +atorvastatin (20 mg) orally. RESULTS: The results showed a significant increase in lipid profile and cardiac biomarkers levels (lactate dehydrogenase, creatine kinase and homocystein), also inflammatory markers, as, tumor necrotic factor alpha and chronic reactive proteins were elevated, moreover, vascular adhesion molecule-1 and nitric oxide synthase were disturbed in high-cholesterol diet compared with normal group. While administration of atorvastatin and functional foods mixture ameliorated these alterations. CONCLUSIONS: Administration of functional foods mixture and atorvastatin were effective in treating hypercholesterolemia, reduce the risk of inflammation and cardiovascular biomarkers with a high safety margin. These efficiencies may be due to its active ingredient that improve the imbalance in the measured biomarkers.

Probiotic mixture improves fatty liver disease by virtue of its action on lipid profiles, leptin, and inflammatory biomarkers.

BACKGROUND: A high fat diet has an essential role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). This condition is characterized by hepatic fat accumulation (steatosis) and is associated with obesity, diabetes, and fibrosis or cirrhosis of the liver. Probiotics may be useful in the treatment of steatosis. This study examined the effects of an ingested probiotic formulation on the lipid profiles, liver functions, leptin levels, and inflammatory marker levels of rats with NAFLD that had been induced via high fat and sucrose diet (HFSD). METHODS: Young male albino rats were randomly divided into three groups: a control group that was fed a standard diet; a second group that was fed a HFSD; and a third group that was given both a HFSD and ingestible probiotic mixtures. The groups were fed these diets for 16 weeks, and were then examined. RESULTS: HFSD-only rats showed hypertriglyceridemia, hypercholesterolemia, and elevated low density lipoprotein (LDL) levels, and their serum alanine transaminase (ALT) and bilirubin levels were significantly higher than those of the control group. Compared to rats on the standard diet, HFSD-only rats showed higher levels of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6), increased serum leptin levels, and increased resistin hormone levels in the adipose tissues. In the third group, the inclusion of the probiotic mixture seemed to ameliorate the effects of the HFSD diet. The NAFD + probiotics group showed improved lipid profiles, better leptin and resistin levels, and better TNF-α and IL-6 levels than the NAFD-only group. They also showed no signs of NAFLD. CONCLUSIONS: The probiotic mixture showed promise as a treatment for NAFLD pathogenesis, and may improve HFSD-induced steatosis through its effects on leptin, resistin, inflammatory biomarkers, and hepatic function markers. We also established that gut microbiota-mediated regulation of lipid profiles was dependent on dietary lipids and carbohydrates.

Antioxidant and Hepatoprotective Efficiency of Selenium Nanoparticles Against Acetaminophen-Induced Hepatic Damage.

Overdoses of acetaminophen (APAP), a famous and widely used drug, may have hepatotoxic effects. Nanoscience is a novel scientific discipline that provides specific tools for medical science problems including using nano trace elements in hepatic diseases. Our study aimed to assess the hepatoprotective role of selenium nanoparticles (Nano-Se) against APAP-induced hepatic injury. Twenty-four male rats were classified into three equal groups: a control group that received 0.9 % NaCl, an APAP-treated group (oral administration), and a group treated with Nano-Se (10-20 nm, intraperitoneal (i.p.) injection) and APAP (oral administration). APAP overdose induced significant elevations in liver function biomarkers, hepatic lipid peroxidation, hepatic catalase, and superoxide dismutase (SOD), decreased the reduced glutathione (GSH) content and glutathione reductase (GR) activity, and stimulated significant DNA damage in hepatocytes, compared to control rats. Nano-Se administration improved the hepatic antioxidant protection mechanism and decreased cellular sensitivity to DNA fragmentation. Nano-Se exhibits a protective effect against APAP-induced hepatotoxicity through improved liver function and oxidative stress mediated by catalase, SOD, and GSH and decreases hepatic DNA fragmentation, a hepatic biomarker of cell death. Nano-Se could be a novel hepatoprotective strategy to inhibit oxidative stress.

Effect of sweetener and flavoring agent on oxidative indices, liver and kidney function levels in rats.

Food additives while attract consumers, improve quality, control weight and replace sugar, may affect seriously children and adults health. Here, we investigated the adverse effects of saccharin and methylsalicyltaes as sweetener and flavoring agent on lipid profile, blood glucose, renal, hepatic function and oxidative stress/antioxidants (lipid peroxidation, catalase and reduced glutathione in liver tissues). Saccharin and methylsalicylate were administered orally in young male albino rats at low and high dose for 30 days. Rats were divided into 5 groups, 1st control group, 2nd and 3rd (low and high saccharin-treated groups) and 4th and 5th (low and high methylsalicylate-treated group). Serum total cholesterol, triglyceride, glucose levels and body weight gain were found decreased in saccharin high dose group compared to control. Rats consumed high dose of saccharin showed a significant decrease in serum triglycerides, cholesterol and LDL levels. Low and high doses of saccharin exhibited a significant increase in liver function marker of ALT, AST, ALP activity, total proteins and albumin levels and renal function test (urea and creatinine levels) in comparison with control group. Further, saccharin at high dose induced significant decrease in liver GSH levels, catalase and SOD activity and increase in hepatic MDA level. Overall saccharin harmfully altered biochemical markers in liver and kidney at higher as well as lower doses. Whereas, methyl salicylates did not pose a risk for renal function and hepatic oxidative markers.

Alterations in lipid profile, oxidative stress and hepatic function in rat fed with saccharin and methyl-salicylates.

BACKGROUND: Food additives attract consumers, improve foods quality, control weight, and replace sugar in foods, while it may affect seriously children and adults health. AIM: To investigate the adverse effects of saccharin and methylsalicyltaes on lipid profile, blood glucose, renal, hepatic function, and oxidative stress/antioxidant (lipid peroxidation, Catalase and reduced glutathione (GSH) in liver tissues). METHODS: 46 young male albino rats were used. Saccharin and methylsalicylate were giving orally as low and high dose for 30 days. Rats were divided into 5 groups, 1(st) control group, 2(nd) and 3(rd) low and high saccharin-treated groups and 4(th) and 5(th) low and high methylsalicylate-treated group. RESULTS: Serum total cholesterol, triglyceride, glucose levels and body weight gain were decreased in saccharin high dose compared to control. Rats ingested high dose of saccharin presented a significant reduction in serum triglycerides, cholesterol and LDL levels. Low and high doses of saccharin exhibited a significant increase in liver function marker of ALT, AST, ALP activity, total proteins and albumin levels and renal function test (urea and creatinine levels) in comparison with control group. Saccharin high dose induce a significant decline in hepatic GSH levels, catalase and SOD activities while increased in hepatic MDA level. CONCLUSION: It could be concluded that, saccharin affects harmfully and alters biochemical markers in hepatic and renal tissues not only at greater doses but also at low doses. Whereas uses of metylsalicylates would not pose a risk for renal function and hepatic oxidative markers.

Oxidative hepatotoxicity effects of monocrotaline and its amelioration by lipoic acid, S-adenosyl methionine and vitamin E.

Liver is the major site for several xenobiotics metabolism, and formation of toxic metabolites that may be hepatotoxic, therefore the burden of metabolism and exposure to dangerous chemicals make liver vulnerable to a variety of disorders. Our work aimed to investigate the effects of some antioxidants such as lipoic acid (LA), S-adenosyl methionine (SAM) and vitamin E in a trail to investigate the possibility of using these substances to relieve and protect liver from exposure to monocrotaline (MCT). Twenty-five mature adult rats were classified into five groups (five rats in each group), control group, MCT-induced hepatic damage, LA+MCT, SAM+MCT and vitamin E+MCT group. Homogenates of liver samples were used for measuring the oxidative biomarkers and hepatic antioxidant status. The results showed that administration of vitamin E, SAM and LA caused a significant increase in liver glutathione contents, glutathione reductase, glutathione peroxidase and glutathione-S-transferase activities and a significant decrease in hepatic catalase and superoxide dismutase. We could conclude that administration of natural LA, SAM and vitamin E before and after MCT injection modulate the hepatic oxidative stresses induced by MCT in various extents.

Impact of breast cancer and combination chemotherapy on oxidative stress, hepatic and cardiac markers.

PURPOSE: Carcinoma of the breast is the most prevalent cancer among Egyptian women and constitutes 29% of National Cancer Institute cases. The aim of this study was to determine the effect of breast cancer on oxidative stress, cardiac markers and liver function tests, moreover the role of 5-fluorouracil, doxorubicin, and cyclophosphamide (FAC) in the treatment of breast cancer and its mechanism through changing the measured markers. METHODS: Forty female breast cancer patients who were admitted to the Department of Oncology of the Beni-Suef University Hospital were enrolled in the study. This study included three arms: a control group of healthy age-matched females (n=20), breast cancer patients who weren't receiving treatment (n=20), and patients undergoing treatment with anticancer combination drugs FAC (n=20). Blood samples collected from the control subjects and patients were analysed to determine levels of catalase, reduced glutathione (GSH), uric acid, nitric oxide (NO), malondialdehyde, creatine kinase (CK), lactate dehydrogenase (LDH), liver enzymes (alanine aminotransferase and aspartate aminotransferase), and creatinine. RESULTS: The levels of catalase and GSH were significantly reduced (p<0.05) in breast carcinoma and FAC treated breast cancer patients. The lipid peroxidation and NO levels were significantly enhanced in both untreated and FAC treated breast cancer patients. The CK and LDH were significantly enhanced (p<0.05) in the FAC group. CONCLUSION: The results from the present study show that oxidative stress is implicated in breast carcinoma and chemotherapy aggravates this oxidative stress which causes damage to many cellular targets and has the main side effect of cardiotoxicity.

Deltamethrin-induced oxidative stress and biochemical changes in tissues and blood of catfish (Clarias gariepinus): antioxidant defense and role of alpha-tocopherol.

BACKGROUND: The pyrethroid class of insecticides, including deltamethrin, is being used as substitutes for organochlorines and organophosphates in pest-control programs because of their low environmental persistence and toxicity. This study was aimed to investigate the impact of commonly used pesticides (deltamethrin) on the blood and tissue oxidative stress level in catfish (Clarias gariepinus); in addition to the protective effect of α-tocopherol on deltamethrin induced oxidative stress. Catfish were divided into three groups, 1st control group include 20 fish divided into two tanks each one contain 10 fish, 2nd deltamethrin group, where Fish exposed to deltamethrin in a concentration (0.75 µg/l) and 3rd Vitamin E group, Fish exposed to deltamethrin and vitamin E at a dose of 12 µg/l for successive 4 days.Serum, liver, kidney and Gills were collected for biochemical assays. Tissue oxidative stress biomarkers malondialdhyde (MDA) and catalase activity in liver, kidney and gills tissues, serum liver enzymes (ALT and AST), serum albumin, total protein, urea and creatinine were analysed. RESULTS: Our results showed that 48 h. exposure to 0.75 µg/l deltamethrin significantly (p < 0.05) increased lipid peroxidation (MDA) in the liver, kidney and gills while catalase activity was significantly decreased in the same tissues. This accompanied by significant increase in serum ALT, AST activity, urea and creatinine and a marked decrease in serum albumin and total proteins. CONCLUSIONS: It could be concluded that deltamethrin is highly toxic to catfish even in very low concentration (0.75 µg/l). Moreover the effect of deltamethrin was pronounced in the liver of catfish in comparison with kidneys and gills. Moreover fish antioxidants and oxidative stress could be used as biomarkers for aquatic pollution, thus helping in the diagnosis of pollution. Administration of 12 µg/l α-tocopherol restored the quantified tissue and serum parameters, so supplementation of α-tocopherol consider an effective way to counter the toxicity of deltamethrin in the catfish.

Effects of panax quinquefolium on streptozotocin-induced diabetic rats: role of C-peptide, nitric oxide and oxidative stress.

BACKGROUND: Insulin-dependent diabetes mellitus are at high risk for vascular disorders as hypertension and nephropathy. Ginseng is one of the most widely used herbal medicines and is reported to have a wide range of therapeutic and pharmacological applications for antioxidant and vasorelaxation although the mechanism is not clear. This study, aimed to evaluate hypoglycemic, antioxidant and vasodilator effects of Panax quinquefolium aqueous ginseng extract (AGE) against streptozotocin (STZ)-induced diabetes in male rats. Furthermore explore the role of AGE in C-peptide and nitric oxide (NO) and their relation in STZ induced diabetic rats. METHODS: Thirty White male Sprague daw-ley rats weighing 150-200 gm, about 4 month old were equally divided into the following: a control group (normal, nondiabetic), a diabetic group induced by intraperitoneal (I/P) injection of STZ (non-AGE-treated) and an AGE-treated diabetic group (STZ+AGE) (for 8 days). Serum level of urea, creatinine, glucose, insulin, C-peptide and NO were analyzed. Activities of hepatic glucose-6-phosphatase (G6Pase), hepatic glycogen phosphorylase and the renal antioxidant enzyme, catalase were analyzed. Also renal oxidative stress marker malondialdehyde (MDA) was measured. RESULTS: Data showed that STZ treated rats produced a significant increased level of serum urea, creatinine, glucose, NO and renal MDA. Also, induced significantly higher activities of hepatic G6Pase and glycogen phosphorylase compared with controls, while give significant lowered serum insulin, C-peptide level and renal catalase activity. Whereas treatment with AGE led to a significant amelioration in the hyperglycemia (lower the activity of G6Pase and glycogen phosphorylase), hyperinsulinemia and oxidative stress markers. Besides declining the higher level of renal function test and NO. CONCLUSIONS: STZ induced-diabetes (DM) associated with renal function disturbances, hypoinsulinemia, defective antioxidant stability and increased (NO) this may have implications for the progress of DM and its related problems. Treatment with AGE improved DM and its associated metabolic problems in different degrees. Furthermore it has insulin sensitizing, hypoglycemic, antioxidant and vasodilator effects. Communally AGE is a potential way to surmount the diabetic state and it has vasodilator effects.