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Pesticides are considered as the most important factors of pollinators’ decline. Imidacloprid (IMD), belonging to Neonicotinoids class, is widely used as a powerful insecticide but generating impor...

The present study aimed to estimate the potential and the molecular mechanism of the hydro-ethanolic extract of O.floribundum against acetaminophen (AC) induced hepatotoxicity. Four groups of female Wistar rats (n=6) was formed to study the hepatoprotective effect of O.floribundum extract against acetaminophen overdose (2 g/kg): Groups N and AC received orally tap water for 03 days and Groups O. floribundum + AC and N+O.floribundum: received orally O. floribundum extract (400 mg/kg). After 1hour (h) of the last dose administered, the paracetamol solution (2 g/kg) is administered orally for group AC and O. floribundum + AC. The hydroethanolic extract of O. floribundum shows strong antioxidant activity “in-vitro”. After 24 h, a single dose of acetaminophen increased significantly serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and the activity of alkaline phosphatase (ALP) significantly and decreased total protein and albumin levels compared to the normal group. These alterations are confirmed by histological observations with inflammation markers (congestion, inflammatory cells infiltration). These observed effects are mainly due to the over-expression of the CYP2E1 and NF_κB genes marked in this study by quantitative RT-PCR. Also, acetaminophen overdose leads to activation of the mitochondrial permeability transition (MPT). leading to hepatocyte necrosis. Pretreatment with O.floribundum before acetaminophen administration removes all previously observed biochemical, histological. and mitochondrial manifestations. These results suggest that O.floribundum has a potent antioxidant power and an interesting hepatoprotective activity against acetaminophen toxicity partly due to the inhibition of CYP2E1 and NF_κB genes expression.

The imidacloprid (IMID) and cypermethrin (CYP) pesticides are known to have neurotoxic effects and negative brain developmental consequences when used separately, but little is known about the consequences of using them as a mixture. That could be passed down from one generation to the next. In this context, we were interested in studying the effect of oral exposure of female rats during gestation and throughout the lactational period to real doses of IMID (1.2 mg/kg) and CYP (6.7 mg/kg) either alone or in a mixture on behavior and mitochondrial redox status. The first and second generation pups were followed from birth to juvenile age using a series of tests to assess reflex, coordination and general motor function, including surface righting, cliff aversion, negative geotaxis and the muscle strength test. At PND 21, cholinergic function, oxidative stress and mitochondrial integrity were assessed in the striatum and hippocampus. Our results showed that IMID and CYP, alone or in combination, induced decreased body weight gain, impaired neurobehavioral performance, and AchE inhibition. Oxidative stress markers including GSH level and SOD, CAT, GST and GPx activities showed a significant decrease. While, lipid peroxidation which was assessed by MDA assay, cytosolic calcium level, swelling and mitochondrial permeability recorded a significant increase. In conclusion, the disruption of mitochondrial redox homeostasis and the presence of neurobehavioral disorders even in the offspring of the F2 generation suggests that independent and combined exposure to IMID and CYP during a critical period of development has irreversible effects; long-lasting and persistent.

Thiacloprid (THI) is a nicotinic receptor agonist widely used as pesticide in Algeria, however it is susceptible to accumulate in various fruits and vegetables and pouring downstream into food plates and contributes to the development of neurodegenerative diseases. Conversely, several natural compounds are provided with cytoprotective potential and, therefore, are able to act against the harmful effects of toxicants such as pesticides. This study focused on striatum (str) and hippocampus (hipp) mitochondrial toxicity assessment, evaluation of behavioral function and intrinsic apoptosis pathway in rats exposed to THI at low-dose (0.020 mg/kg) for 3 months. In addition, this study examined neuroprotective potential of bitter apricot kernel extract when administered concomitantly with THI at the dose of 50 mg/kg. In current study, assessment of mitochondrial permeability transition pore (mPTP) and swelling, evaluation of mitochondrial redox status, cholinergic function (Ach E) and apoptosis markers (Caspase 9 and 3, Bax and Bcl2, Cytochrome c and cytosolic calcium) were performed in both brain areas, besides behavioral and histopathological examination. The results showed an increase of lipid peroxidation in both of str and hipp with a values of 1,14 ± 0,04 nmol/mg of proteins (pr) and 1,58 ± 0,09 nmol/mg pr. respectively and a significant decrease in GSH (0,09 ± 0,01 mmol/mg pr. in hipp and 0,08±0,01 mmol/mg pr. in str), the results also showed a change in the activity of antioxidants enzymes SOD (16,37±1,09 UI/mg pr. in hipp14,54±1,46 UI/mg pr. in str) , CAT (0,010±0,01 UI/mg pr. in hipp and 0,005±0,004 UI/mg pr. in str), GPx (0,01± 0,001 nmol/mg pr. in both hipp and str) and GST (23,73±1,68 UI/mg pr. in hipp and 17,56± 1,04 UI/mg pr. in str), as well as an abrupt increase in mPTP opening with a value of (0,057±0,005 in str and 0,054±0,005 in hipp) , which leaded to mitochondrial swelling where the level o mitochondrial swelling was (0,016±0,002 in str and 0,106±0,003 in hipp), the swelling was associated also with a high releasing of Cyt-c with a values of (4,48 ± 1,26 µg/ml in str and 5,32 ± 1,08 µg/ml in hipp ) and Ca++( 2,26±0,06 mmol/l in str and 2,32±0,07 mmol/l in hipp) into the cytosol, the results also showed a significant decreasing of Bcl2 (16,4 ± 1,86 ng/mg pr in str and 14,8± 0,82 ng/mg pr in hipp), in the other hand the rates of caspase-9 were (278±14 mAbs/mg pr.) in str and 212 ±24 mAbs/mg pr. in hipp), caspase3 (184± 16mAbs/mg pr.) in str and 250 ±14mAbs/mg pr. in hipp), and BAX (0,926 ng/mg pr in str and 1,189 ng/mg pr in hipp) were increased. The results of this study revealed also a decrease of memorization processes and learning abilities, at the same time a decrease in Ach E activity (14,02± 0,78 nmol/min/mg pr. in str and 22,35± 1,77 nmol/min/mg pr. in hipp) was recorded. Inversely, bitter apricot kernels extract showed higher cytoprotective potential against THI neurotoxicity, since mitochondrial redox homeostasis and membrane integrity were recovered, cognitive impairment and brain tissue damage were also prevented. In conclusion, THI induced mitochondrial disorders, triggered apoptosis signaling pathway and impaired cognitive functions which were prevented by bitter apricot kernels extract when associated with this pesticide.

The extensive use of Lambda-cyhalothrin (LCT) has been associated with the various toxicities that non-target organisms can undergo including mammals. However, the mechanism of induced-LCT cytotoxicity in animal brain cells is still elusive, particularly in brain regions, notably the hippocampus, an area directly involved in cognitive function. This study aimed to investigate the neurotoxic effects in the rat hippocampus chronically exposed to LCT (0.18 mg/kg and 0.36 mg/kg), and the neuroprotective potential of Melissa officinalis L methanol extract (MOE) (200 mg/kg) against this toxicity. After experimental period (90 days), the redox status, the functional and structural integrity of the hippocampus mitochondria as well as the apoptotic signaling pathway were evaluated. The current findings suggest that LCT produces imbalance of mitochondrial redox status expressed by, on one side, increasing of stress markers such as protein carbonyls (PCO), malondialdehyde (MDA), and hydrogen peroxide (H2O2) levels; and on the other side, by a decline in the potential of antioxidant systems, namely the level of mitochondrial enzymatic activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD) and glutathione (GSH).This study also showed an increase in mitochondrial permeability, along with mitochondrial edema and considerable decrease in its O2 consumption. Moreover, the same results recorded an increase in caspase-3 and cytosolic cytochrome-c. Conversely, this study proved that all these toxic aspects induced by LCT were significantly mitigated when the administration of this synthetic pyrethroid was associated with MOE. Taken together, data of this study shed light on mitochondrial damage and apoptosis stimulation under the toxic effect of LCT and suggests that MOE is endowed with potent neuroprotective effect, possibly via its antioxidant and antiapoptotic properties.

The increase in the usage of silica nanoparticles (SiNPs) in the industrial and medical fields has raised concerns about their possible adverse effects on human health. The present study aimed to investigate the potential adverse effects of SiNPs at daily doses of 25 and 100mg/kg body weight intraperitoneally (i.p.) for 28 consecutive days on markers of liver damage in adult male rats. Results revealed that SiNPs induced a marked increase in serum markers of liver damage, including lactate dehydrogenase (LDH), alanine aminotransferase (ALAT), and aspartate aminotransferase (ASAT). SiNPs also induced an elevation of reactive oxygen species (ROS) production in liver, along with an increase in oxidative stress markers (NO, MDA, PCO, and H2O2), and a decrease in antioxidant enzyme activities (CAT, SOD, and GPx). Quantitative real-time PCR showed that SiNPs also induced upregulation of pro-apoptotic gene expression (including Bax, p53, Caspase-9/3) and downregulation of anti-apoptotic factors Bcl-2. Moreover, histopathological analysis revealed that SiNPs induced hepatocyte alterations, which was accompanied by sinusoidal dilatation, Kupffer cell hyperplasia, and the presence of inflammatory cells in the liver. Taken together, these data showed that SiNPs trigger hepatic damage through ROS-activated caspase signaling pathway, which plays a fundamental role in SiNP-induced apoptosis in the liver.

Cypermethrin (CYP) and Acetamiprid (AC) are two pesticides widely used in Algeria to eliminate insects that spoil crops and transport disease. In this study, the neurobehavioral effects induced by a mixture of the pesticides (CYP+AC) were tested at doses of 3.14 and 0.32 mg/kg for three months. The evaluation of mitochondrial oxidative stress on striatum tissues was recorded. According to the main results, CYP+AC mixture led to the disruption of mitochondrial parameters evaluated by a significant increase of MDAmit level, of GSTmit and SODmit activities, and a significant decrease of GSHmit level, CATmit and GPxmit activities. Due to disruption of some of mitochondria antioxidant enzymes, which may be the main cause of brain cell degeneration and decrease of learning and memorizing rate, the administration of CYP+AC mixture induced neurotoxicity.

Cadmium (Cd) is a highly toxic heavy metal. It accumulates in biological tissues, especially in fish which constitutes a first rank food for humans, particularly in the coastal areas. This study investigates the effect of long-term exposure to low Cd concentration (17 μg/kg/day) in rat striatum and hippocampus. In this study, the neurobehavioral ability changes were assessed by applying cognitive standard testing at the end of the rats’ exposure period. In addition, the examination of mitochondrial swelling was performed at the same time of evaluation of its redox status in the brain regions studied through stress parameters (GSH, MDA, GST, and CAT). This study examined also whether this long-term exposure can modify the apoptotic signaling pathway via assessment of apoptotic markers (caspase-8 and 9, Bax, Bcl-2, and Cyt-c) in cell lysates. The results of this study showed changes in neurobehavioral abilities of animals and a stronger mitochondrial swelling associated with a significant decrease in antioxidant systems (GSH, GST, and CAT) and conversely an increase in the lipoperoxidation end product (MDA) in both the striatal and hippocampal mitochondria. In addition, the results revealed a significant increase in pro-apoptotic intracellular components such as caspase-9, Cyt-c, and Bax, and showed also an evident decrease in Bcl-2 levels. In conclusion, our results reported that chronic exposure to Cd produces behavioral and cognitive perturbations, enhances oxidative stress associated with mitochondrial edema and Cyt-c leakage, and, ultimately, potentiates apoptosis signaling pathway in both brain regions in rats.

Pesticides are chemicals used to fight agricultural pests. Their use causes extensive damage to both humans and animals, resulting in diseases mainly affecting the respiratory and digestive systems. Through this study, we evaluated the pneumotoxicity caused by a deltamethrin (DM) insecticide at a dose of 0.64mg.kg-1.day-1. We also evaluated the preventive and curative effect of the medicinal plant "citrullus colocynthis. L" antagonist of this toxicity at a dose of 150mg.kg-1.day-1. We carried out the experimental application on Wister rats as an animal model of exhalation. Several experiments were carried out on the activity of enzymes and vital indicators. This study revealed a decrease in the concentration of the protein accompanied by a decrease in the means of development of the body [25±0.23]. Then, our study showed that DM has an oxidative effect, resulting in a decrease in the level of GSH [0.05 ±0.00] and the enzymatic activity of GPx [0.34±0.05]. In addition to an increase in the level of MDA [4.90±0.72] and the enzymatic activity of GST [0.84±0.11]. In addition, the histological study carried out on a fragment of lung of rats treated with this pesticide showed changes in the histological structure of the lungs resulting in vascular congestion, infiltration of inflammatory cells, thickening of the walls of blood vessels, as we do. Observed intra-alveolar hemorrhages and hyperplasia of the alveolar lining. On the other hand, we have confirmed the preventive effect of the citrullus colocynthis. L after treatment with this pesticide, which has an anti-oxidant activity, which can reduce the intensity of the oxidative stress resulting from deltamethrin and its effectiveness. In the treatment of lung, tissue effected by this pesticide and it is stored in its natural state.

The existence of numerous side effects following the use of anti-inflammatory drugs has led to the present study about Mentha rotundifolia L. The plant is prescribed in folk medicine treatment of inflammatory diseases to discover biomolecules that have substantial beneficial effects with the least adverse effects. In this study, the anti-inflammatory and analgesic effects of polyphenols from Mentha rotundifolia L . leaves extract were evaluated, using carrageenan-induced mice paw edema model and acetic acid induced writhing method. The effects on oxidative stress of plant extract were also evaluated after sacrifice of the experimental mice. The extract showed a dose dependent effect on inflammation inhibition. The highest percentage of edema inhibition was 84.49% after 4 h at dose of 600 mg/kg. The extract showed a significant ( p p Mentha rotundifolia L . possesses anti-inflammatory and analgesic activities. It possesses also in vivo antioxidant activity and can be employed in protecting tissue from oxidative stress.

This study focuses on evaluation of the toxic effect of enduslfan (END) and the quercetin (QUE) role in rat striatum. END (2 mg/kg) associated or not with QUE (10 mg/kg), was daily administered to animals during 6 days. Then, striatum mitochondria suspension was prepared by centrifugation to assess mitochondria swelling and redox status by determining malondialdehyde (MDA), glutathione-s-transferase (GST), catalase (CAT) and Glutathion (GSH). In addition, striatal lysate was also elaborated to determine apoptosis markers caspases-9 and 8; B-cell lymphoma2 (Bcl2) and Bcl2 associated X (Bax), by applying luminescence and ELISA methods. This study has shown an increase in mitochondria swelling and induction of apoptotic pathway. In addition, a decrease in mitochondrial enzymatic activity of GST and CAT was recorded as well as an increase in mitochondrial MDA rate and a fall in mitochondrial GSH level. By contract, QUE has maintained oxidative stress and apoptotic markers at their homeostasis levels and prevented striatum mitochondria swelling. Thus, endosulfan impairs redox status and membrane integrity of striatum mitochondria and induces apoptosis, but the use of QUE avoids these alterations.

Objective The current study aimed at evaluating in Albino mice the analgesic, anti-inflammatory, and antioxidant effects of Achillea odorata ; a medicinal plant commonly used in Algerian folk medicine to provide scientific basis for its use. Methods The biological tests were performed on aqueous extracts. Antinociceptive activity was estimated using acetic acid that induces algesia in mice. Anti-inflammatory activity was investigated using carrageenan-induced paw edema method and the antioxidant effect was performed using MDA, GSH, CAT and SOD estimations. Results The study of the analgesic activity of the A . odorata polyphenolic extract showed a very potent analgesic activity with an ability to inhibit abdominal cramps similar to that of positive control. In addition, evaluation of edema inhibition percentage showed that plant extract has a significant anti-inflammatory activity. In addition, the extract has the ability to modulate the redox potential in vivo , induced by inflammation, which has been demonstrated by the determination of GSH, MDA, CAT and SOD. Conclusions Our results suggest that A . odorata possesses potential antinociceptive, anti-inflammatory and antioxidant compounds which could be tested as drug candidates against oxidative and inflammation-related pathological processes.

Metformin therapy is associated with lower serum magnesium (Mg2+) levels in type 2 diabetes patients. The TRPM6 channel determines the fine-tuning of Mg2+ (re)absorption in intestine and kidney. Therefore, we aimed to investigate the short- and long-term effects of metformin on TRPM6. Patch clamp recordings and biotinylation assays were performed upon 1 h of incubation with metformin in TRPM6-transfected HEK293 cells. Additionally, 24 h of treatment of mDCT15 kidney and hCaco-2 colon cells with metformin was applied to measure the effects on endogenous TRPM6 expression by quantitative real-time PCR. To assess Mg2+ absorption, 25Mg2+ uptake measurements were performed using inductively coupled plasma mass spectrometry. Short-term effects of metformin significantly increased TRPM6 activity and its cell surface trafficking. In contrast, long-term effects significantly decreased TRPM6 mRNA expression and 25Mg2+ uptake. Metformin lowered TRPM6 mRNA levels independently of insulin- and AMPK-mediated pathways. Moreover, in type 2 diabetes patients, metformin therapy was associated with lower plasma Mg2+ concentrations and fractional excretion of Mg2+. Thereby, short-term metformin treatment increases TRPM6 activity explained by enhanced cell surface expression. Conversely, long-term metformin treatment results in downregulation of TRPM6 gene expression in intestine and kidney cells. This long-term effect translated in an inverse correlation between metformin and plasma Mg2+ concentration in type 2 diabetes patients.

Aim The current study was designed to investigate the antidiabetic and hypolipidemic properties of the 80% methanolic leaves extract of Pistachia lentiscus L., a medicinal plant commonly used in Algerian folk medicine for the treatment of diabetes. Methods We evaluated the effects of P. lentiscus L. leaves extract on blood glucose, cholesterol, triglycerides and insulin levels in alloxan-induced diabetic rats. The effects of the extract on α-amylase, sucrase and glucose uptake by yeast cells in vitro were also evaluated. For qualitative determination of biologically active compounds, RP-HPLC analysis of the extract was carried out. Results P. lentiscus L. extract exhibited a significant decrease in blood glucose as well as cholesterol and triglyceride levels and caused a significant increase in plasma insulin. In addition, it significantly increased glucose uptake in yeast cells and inhibited α-amylase and sucrase activities. Conclusion Based on its strong antidiabetic activity, P. lentiscus L. extract appears to be a potential herb for the treatment of diabetes and can be further explored for isolating the active component(s).

Persistent organic pollutants (POPs) are long-lived organic compounds that are considered one of the major risks to ecosystem and human health. Recently, great concerns are raised about POPs mixtures and its potential toxicity even in low doses of daily human exposure. The brain is mostly targeted by these lipophilic compounds because of its important contain in lipids. So, it would be quite interesting to study the effects of exposure to these mixtures and evaluate their combined toxicity on brain cells. The present study was designed to characterize the cognitive and locomotors deficits and brain areas redox status in rat model. An orally chronic exposure to a representative mixture of POPs composed of endosulfan (2.6 μg/kg), chlorpyrifos (5.2 μg/kg), naphthalene (0.023 μg/kg) and benzopyrane (0.002 μg/kg); the same mixture with concentration multiplied by 10 and 100 was also tested. Exposed rats have shown a disturbance of memory and a decrease in learning ability concluded by Morris water maze and the open field tests results and anxiolytic behaviour in the test of light/dark box compared to control. Concerning brain redox homeostasis, exposed rats have shown an increased malondialdehyde (MDA) amount and an alteration in glutathione (GSH) levels in both the brain mitochondria and cytosolic fractions of the cerebellum, striatum and hippocampus. These effects were accompanied by a decrease in levels of cytosolic glutathione S-transferase (GST) and a highly significant increase in superoxide dismutase (SOD) and catalase (CAT) activities in both cytosolic and mitochondrial fractions. The current study suggests that environmental exposure to daily even low doses of POPs mixtures through diet induces oxidative stress status in the brain and especially in the mitochondria with important cognitive and locomotor behaviour variations in the rats.

Approximately 30% of patients with type 2 diabetes mellitus (T2D) have hypomagnesemia (blood magnesium (Mg2+) concentration 2+ levels. To investigate how T2D and metformin affect Mg2+ homeostasis db/m and db/db mice were treated with metformin or placebo. Mice were housed in metabolic cages to measure food and water intake, and to collect urine and feces. Serum and urinary Mg2+ concentrations were determined and mRNA expression of magnesiotropic genes was determined in kidney and distal colon using RT-qPCR. Db/db mice had significantly lower serum Mg2+ levels than db/m mice. Mild hypermagnesuria was observed in the db/db mice at two weeks, but not at four weeks. Metformin-treatment had no effect on the serum Mg2+ concentration and on the urinary Mg2+ excretion. Both in kidney and distal colon of db/db mice, there was a compensatory upregulation in the mRNA expression of magnesiotropic genes, such as transient receptor potential melastatin 6 (Trpm6), whereas metformin treatment did not affect gene expression levels. In conclusion, we show that T2D causes hypomagnesemia and that metformin treatment has no effect on Mg2+ homeostasis in mice.

Pyrethrino < ds are synthetic pesticides widely used in agriculture and farms to protect crops from weeds, insects, fungi, and molds. Increased and uncontrolled use of these pollutants can have harmful effects on human health via consumption of contaminated food products. In the present study, deltamethrin (DLT = 3.72 mg/kg) and Bifenthrin (BF = 2.6 mg/kg) were used during a long-term exposition in the rats to assess their effect on mitochondrial integrity and function in different brain areas (hippocampus, striatum, cortex, and cerebellum). The results of this study have shown that chronic treatment of rats by both DLT and BF, on their own or in a mixture, has induced a significant increase in mitochondrial MDA, but when quercetin (Que) was co-administered with pesticides, this enhancement has been prevented in the almost of treated rats compared to solvent and control groups. In hippocampus area, GSH has significantly increased in all treated rats, except for BF and DLT-Que.-treated groups. In striatum, GSH has been depleted in the BF and DLT-treated groups compared to control and solvent groups; in contrast, when Que. was associated with pesticides, the rate of this tripeptide has been maintained at normal levels. In the cortex and cerebellum, GSH has been depleted significantly in all treated animals but has increased in DLT-Que. and mixture-Que.-treated groups in the cerebral cortex, at the same time; it has been maintained at normal levels in BF-Que.-treated groups in the cerebellum compared to control and solvent rats. On the other side, the results of this study have shown a loss of catalase (CAT) and glutathione S-transferase (GST) activities in all brain regions of pesticide-treated rats, but such a fall in enzymatic activities has been prevented by Que. when it was co-administered to rats with pesticides at the dose of 5 mg/kg, except in the cerebellum. In addition, this study has shown mitochondria's swelling in almost all the brain areas with exception of the cerebellum, providing information about a loss of mitochondrial membrane integrity in brain neurons of rats exposed to pyrethrino < ds. Furthermore, preventive administration of Que., in association with pesticides (5 mg/kg) or their mixture (10 mg/kg), has prevented mitochondria swelling in almost all of the analyzed brain tissues.

The present work is to evaluate the neurotoxicity induced by pyrethroid insecticide “Deltamethrin” at 0.32 mg/kg/day in two main regions of the Wistar rat brain (hippocampus and striatum) and the protective effects of Quercetin at 10 mg/kg/day on this toxicity after 90 days of exposure. The assay of brain parameters showed that Deltamethrin caused a significant increase of mitochondrial metabolite level (proteins, lipids, and carbohydrates) and enzyme activity (glutathione S-transferase and superoxide dismutase); a decreased amount of mitochondrial glutathione level and catalase and glutathione peroxidase activities; and an increase of malondialdehyde (MDA) acid levels of the two regions. Furthermore, mitochondrial functional testing in the brains of treated rats exhibited a significant increase in permeability followed by a mitochondrial swelling. Instead, a statistically significant decrease in mitochondrial respiration (O2 consumption) was recorded in the striatum and hippocampus. Our study showed that the pesticide caused a significant increase of the cytochrome c amount correlated with activation of neuronal apoptosis mechanisms by the significant increase of caspase-3 of hippocampus and striatum. In particular, the results of behavioral tests (open field, classic maze tests of sucrose, and Morris water maze) have significant changes, namely bad behavior of the treated rats, affecting the level of anxiety, learning, and memory, and general motor activity has mainly been shown in treated rats. In addition, the histological cuts clearly confirm cerebral necrosis in the hippocampus and the striatum caused by the pesticide. They allow us to consider the necrotic areas, black spots, reduction, and denaturation of these brain regions in the treated rats. On the other hand, we have studied the protective effects against the neurotoxicity of Deltamethrin (DLM). In this context, after the gavage of Quercetin at the dose of 10 mg/kg/day, we have noticed an improvement in the entire parameters: mitochondrial enzyme, metabolic, histological, and behavioral parameters. This confirmed the improvement of preventive and curative effect of Quercetin against free radicals induced by the DLM.

Les effets antidiabetogene et cytoprotecteur des extraits de flavonoides de Ranunculus repens L. et de la quercetine sont etudies dans le cas du diabete induit par l’alloxane chez les rats Wistar albinos. Ces composes phenoliques se sont montres d’un potentiel cytoprotecteur des cellules β et d’une capacite antidiabetogene dans le diabete alloxanique qui desequilibre le statut redox des cellules pancreatiques au profit du stress oxydatif. L’activite de ces flavonoides se traduit par un effet significativement positif sur l’insulinosecretion des cellules β et la glycemie. Cet effet est du au pouvoir antioxydant et cytoprotecteur des composes phenoliques porte sur les cellules β intoxiquees par l’alloxane se traduisant par la reduction de la production du MDA en empechant donc la lipoperoxydation et la normalisation du niveau cytosolique des systemes antioxydants (SOD, CAT et GSH). Ces effets sont susceptibles de maintenir, par consequent, un statut redox cellulaire en equilibre apres l’administration de l’alloxane en association aux flavonoides.

Anticancer therapy with epirubicin (EPI) results in acute hepatotoxicity, likely due to the generation of free radicals. However, the oxidative status of rat liver cells and mitochondria after EPI toxicity has not been investigated. In the present study, we first investigated the pro-oxidant effect of EPI on both hepatic cells and mitochondrial function. Injection of EPI into rats at a dose of 9 mg/kg (cumulative dose in human chemotherapy), induced hepatic dysfunction, as revealed by a significant increase in serum glutamate oxaloacetate transaminases (SGOT) and glutamate pyruvate transaminases (SGPT). Oxidative stress in liver cells and mitochondria was provoked by EPI because a statistically significant reduction of catalase (CAT), superoxide dismutase (SOD) and cytosolic glutathione (GSH) levels, and a significant increase in malonedialdehyde (MDA) levels – an indicator of lipid peroxidation that can perforate biological membranes – were observed. Second, the protective effect of quercetin (QE) (0.33 mg/kg) against EPI-induced oxidative stress was also investigated. Indeed, the pretreatment of rats with QE protected liver cells and mitochondria from oxidative stress. This treatment prevented hepatic dysfunction by maintaining normal levels of serum transaminases following the inhibition of their hepatic leakage by preventing lipid peroxidation. Thus, QE works through the prevention of cellular membrane perforation and the antioxidant defense system of mitochondria from liver cells, which represent compartments for the permanent production of reactive oxygen species (ROS) through the respiratory chain.

Erratum to: Neurobehavioral deficits and brain oxidative stress induced by chronic low exposure of persistent organic pollutants mixture in adult female rat

The objective of this work is to study the opposite effect of Selenium on the toxicity induced by zinc in rabbits (Oryctolagus cuniculus). Twenty rabbits were given repeated per os (p.o.) administration, five with zinc chloride at 0.24 mg/Kg/day, five with 0.05 μg/kg/day of selenium, five with mixture (ZnCl2/Se) 0.24mg/kg+0.05μg/kg/day and five rabbits served as controls. In the present study, Hepatotoxic effect of zinc chloride translated by a decrease of body weight (weight gain), a decreased of lipid rate, an increased in carbohydrate amount and proteins level in the liver. The pro-oxidant effect of zinc chloride on hepatocytes was first investigated. The gavage of ZnCl2 into rabbits at the dose of 0.24 mg/kg/day, induced stress by a significant reduction of GST, CAT and glutathione peroxidase (GPx) activity, glutathione (GSH) level. In addition, a significant increase in malonedialdehyde (MDA) levels was observed, (index of lipid peroxidation). On the other hand, the supplementation of selenium (Se) 0.05 μg/kg/day orally in rabbits treated with zinc has improved some biochemical parameters and decreased the other harmful effects of zinc; selenium seems to be a simple and effective antioxidant to reduce the imbalance state between the formation of free radicals and antioxidant systems.

Recent toxicological studies have demonstrated that exposure to organochlorine pesticides is susceptible to produce various alterations in brain cell which significantly contribute to a loss in neurobehavioral skills and disturbance of neuronal function. Acetamipride (AC) is belonging to this organochlorines family and it is considered less harmful by toxicovigilance systems and practices in Algeria. The aim of this work was mainly to evaluate the impact of this pesticide on the brain cell integrity and function in Acetamiprid-treated rats at the dose of 3.14 mg/kg (1/60 Lethal Dose) daily during 3 months. Several indicators of neuronal apoptosis and function have been rated, in addition to classical labyrinth and Maze tests monitoring to evaluate learning and memorization abilities in rats exposed to this neonicotinoid. The results of this study have shown significant enhancing of cytochrome-c (p