Laboratory of Aggression Physiology and Endocrine Metabolic Studies

Tunis, Tunisia

Laboratory of Aggression Physiology and Endocrine Metabolic Studies

Tunis, Tunisia

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El-Bini Dhouib I.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | Annabi A.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | Jrad A.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | El-Golli N.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | And 3 more authors.
General physiology and biophysics | Year: 2015

Carbosulfan (CB)-induced oxidative stress leads to the inevitable accumulation of free radicals and eventual alteration of antioxidant enzymes in various biological systems. The present study is designed to investigate the preventive effect of N-acetylcysteine (NAC) on carbosulfan-induced hepatic and renal dysfunction in rats. Rats exposed to CB and NAC were examined for toxicity by assessing various biochemical alteration and stress markers including in liver and kidney. Significant increases of blood alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma glutamyltransferase (GGT), creatinine and urea were detected in CB-treated rats. In addition, the levels of antioxidative enzymes such as catalase (CAT), superoxide dismutase (SOD) and reduced glutathione (GSH) also were assessed. According to the results, rats exposed to carbosulfan showed a significant increase in the accumulation of stress markers and an alteration in the antioxidative enzymes activity, when compared to their respective controls. Interestingly, administration of NAC to CB-treated rats attenuates the toxicity of this compound, objectified by biochemical and oxidative improvement of liver and kidney. Thus, the present study reports for the first time that NAC could be a promising therapeutic agent against CB induced oxidative stress.


Lasram M.M.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | Dhouib I.B.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | Dhouib I.B.,Pasteur Institute of Tunis | Bouzid K.,Charles Nicolle Hospital | And 7 more authors.
Environmental Toxicology and Pharmacology | Year: 2014

Insulin resistance and risk of type 2 diabetes are the most important complications following exposure to organophosphorous (OPs) pesticides. Regarding the importance of liver on metabolic pathways regulation, in particular blood glucose homeostasis, we focused on liver inflammation and oxidative damages in a subchronic model of toxicity by malathion. Adult male Wistar rats of body weight 200-250g were used for the study. Malathion (200mg/kg b.w./day) was administered to rats by oral intubation for 28 days. Glycemic and insulin resistance indices, markers of liver injury, markers of inflammation and oxidative stress were assessed. Malathion-treated rats showed increased glycemia, insulinemia and glycated hemoglobin level, HOMA-IR and HOMA-β indices, plasma activities of hepatocellular enzymes, lipid peroxidation index, CD3+/CD4+ and CD3+/CD4+ and pro-inflammatory cytokines when decreased antioxidant status in liver was noted. Most of our study indicates that malathion promotes insulin resistance, inflammation and Hepatosteatosis in subchronic model of exposure. On the basis of biochemical and molecular findings, it is concluded that insulin resistance induced by malathion occurs through oxidative stress and related pro-inflammatory markers in a way to result in a reduced function of insulin in liver cells. © 2014 Elsevier B.V.


El-Bini Dhouib I.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | Lasram M.M.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | Annabi A.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | Gharbi N.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | El-Fazaa S.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies
Pesticide Biochemistry and Physiology | Year: 2015

Organophosphorus (OP) and carbamate (CM) pesticides are widely used in agriculture. These pesticides are highly toxic to humans and their residues in food pose potential threat to human health. In this comparative study, we investigated the effect of subchronic exposure of OPs (malathion, MAL) and CM (Carbosulfan, CB) on rat liver and spleen. Biochemical analysis showed that levels of hepatic enzymes (ALT, ALP, LDH and PAL) changed after exposure to the pesticides. In the liver extracts, lipid peroxidation index increased after the treatment by pesticides. Our results indicated that exposure to MAL and CB leads to alteration of liver redox status. Both pesticides induced focal inflammation and fibrosis in the liver. After subchronic administration of MAL (200 mg/kg) and CB (25 mg/kg), systemic inflammation, as depicted by the increase in IFN-δ activity in liver, was observed in both malathion and carbosulfan treated animals. In addition, the results showed that MAL significantly increased TCD4+ and TCD8+ lymphocyte number. It also decreased INF-δ and IL-4 production. However, CB induced a reduction of TCD8+ number and cytokine production in spleen cells. In conclusion, malathion and carbosulfan had significant immunomodulatory properties in the spleen with inflammation and oxidative stress induction in the liver. © 2015 Elsevier Inc.


Selmi S.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | Tounsi H.,Institute Pasteur Of Tunis 13 | Safra I.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | Abdellaoui A.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | And 3 more authors.
RSC Advances | Year: 2015

We aimed in the present work to evaluate the implication of oxidative stress in the toxicological effects of subchronic malathion exposure on reproductive function in mice. In this respect, we used prepubertal male mice separated into two groups: a control and a malathion treated group. Animals were treated by gavage (per orally, p.o.) with malathion at 200 mg kg-1, body weight (b.w.) during thirty days. We found that malathion treatment leads to the alteration of semen parameters such as a decrease of testosterone level and acetylcholinesterase activity, an induction of apoptosis and necrosis in spermatozoa as well as a decrease of reproductive performance of male mice. The histopathological examination showed a marked change in the testis tissue. Malathion intoxication was by an increase of malondialdehyde (MDA) level, a decrease of sulfhydril groups (-SH) content, as well as a depletion of antioxidant enzyme activities such as catalase (CAT), total superoxide dismutase (SOD), Cu/Zn-SOD and Mn-SOD in testis and epididymis. More importantly, malathion treatment clearly induced a decrease in mRNA expression of COX isoenzyme in cauda and epididymis as well as GPx-4 in testis and GPx-5 in epididymis. These data suggest that a marked deregulation of reproductive function in prepubertal male mice exposed to malathion might be partly due to pro-oxidant properties of the examined compound. This journal is © The Royal Society of Chemistry 2015.


Lasram M.M.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | El-Golli N.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | Lamine A.J.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | Douib I.B.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | And 5 more authors.
General and Comparative Endocrinology | Year: 2015

Organophosphorus pesticides are known to disturb glucose homeostasis and increase incidence of metabolic disorders and diabetes via insulin resistance. The current study investigates the influence of malathion on insulin signaling pathways and the protective effects of N-acetylcysteine (NAC). Malathion (200. mg/kg) and NAC (2. g/l) were administered orally to rats, during 28 consecutive days. Malathion increases plasma glucose, plasma insulin and glycated hemoglobin levels. Further, we observed an increase of insulin resistance biomarkers and a decrease of insulin sensitivity indices. The GP, GSK3β and PEPCK mRNA expressions were amplified by malathion while, the expression of glucokinase gene is down-regulated. On the basis of biochemical and molecular findings, it is concluded that malathion impairs glucose homeostasis through insulin resistance and insulin signaling pathways disruptions in a way to result in a reduced function of insulin into hepatocytes. Otherwise, when malathion-treated rats were compared to NAC supplemented rats, fasting glucose and insulin levels, as well as insulin resistance indices were reduced. Furthermore, NAC restored liver GP and PEPCK expression. N-acetylcysteine showed therapeutic effects against malathion-induced insulin signaling pathways disruption in liver. These data support the concept that antioxidant therapies attenuate insulin resistance and ameliorate insulin sensitivity. © 2014 Elsevier Inc.


Alya A.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | Ines D.B.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | Montassar L.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | Najoua G.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies | Saloua E.F.,Laboratory of Aggression Physiology and Endocrine Metabolic Studies
Iranian Journal of Basic Medical Sciences | Year: 2015

Objective(s): Lead (Pb) is a toxic metal inducing many destructive effects leading to a broad range of physiological, biochemical, and neurological dysfunctions in humans and laboratory animals. Materials and Methods: Here, we investigated the effect of chronic exposure to Pb (50 mg/l) on oxidative stress, hepatotoxicity, nephrotoxicity, and lipid profile of two different age groups of female rats treated with Pb from delivery until puberty period (40 days, Pb40) and post puberty period (65 days, Pb65). Results: Our results clearly show that the administration of Pb produces oxidative damage in liver and kidney, as strongly suggested by the significant increase in TBARS, decrease in total SH, and the alteration of SOD activity. Elevation in liver function biomarkers, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and reduction in total protein (liver and plasma) and albumin are evidence of perturbations of liver synthetic function. In young Pb‐treated group, Pb‐induced nephropathy was more pronounced by the increase in the levels of creatinine, urea, and uric acid. However, hyperlipidemia was evident for both Pb‐exposed groups leading to a potential risk for cardiovascular diseases and atherosclerosis. Conclusion: It is concluded that Pb induces metabolic and oxidative disturbances depending on the age of the animals, which are not negligible. © 2015, Mashhad University of Medical Sciences. All rights reserved.


PubMed | Charles Nicolle Hospital, Laboratory of Aggression Physiology and Endocrine Metabolic Studies and Pasteur Institute of Tunis
Type: Journal Article | Journal: Environmental toxicology and pharmacology | Year: 2014

Insulin resistance and risk of type 2 diabetes are the most important complications following exposure to organophosphorous (OPs) pesticides. Regarding the importance of liver on metabolic pathways regulation, in particular blood glucose homeostasis, we focused on liver inflammation and oxidative damages in a subchronic model of toxicity by malathion. Adult male Wistar rats of body weight 200-250g were used for the study. Malathion (200mg/kg b.w./day) was administered to rats by oral intubation for 28 days. Glycemic and insulin resistance indices, markers of liver injury, markers of inflammation and oxidative stress were assessed. Malathion-treated rats showed increased glycemia, insulinemia and glycated hemoglobin level, HOMA-IR and HOMA- indices, plasma activities of hepatocellular enzymes, lipid peroxidation index, CD3(+)/CD4(+) and CD3(+)/CD4(+) and pro-inflammatory cytokines when decreased antioxidant status in liver was noted. Most of our study indicates that malathion promotes insulin resistance, inflammation and Hepatosteatosis in subchronic model of exposure. On the basis of biochemical and molecular findings, it is concluded that insulin resistance induced by malathion occurs through oxidative stress and related pro-inflammatory markers in a way to result in a reduced function of insulin in liver cells.


PubMed | Laboratory of Aggression Physiology and Endocrine Metabolic Studies
Type: | Journal: Pesticide biochemistry and physiology | Year: 2015

Organophosphorus (OP) and carbamate (CM) pesticides are widely used in agriculture. These pesticides are highly toxic to humans and their residues in food pose potential threat to human health. In this comparative study, we investigated the effect of subchronic exposure of OPs (malathion, MAL) and CM (Carbosulfan, CB) on rat liver and spleen. Biochemical analysis showed that levels of hepatic enzymes (ALT, ALP, LDH and PAL) changed after exposure to the pesticides. In the liver extracts, lipid peroxidation index increased after the treatment by pesticides. Our results indicated that exposure to MAL and CB leads to alteration of liver redox status. Both pesticides induced focal inflammation and fibrosis in the liver. After subchronic administration of MAL (200 mg/kg) and CB (25 mg/kg), systemic inflammation, as depicted by the increase in IFN- activity in liver, was observed in both malathion and carbosulfan treated animals. In addition, the results showed that MAL significantly increased TCD4+ and TCD8+ lymphocyte number. It also decreased INF- and IL-4 production. However, CB induced a reduction of TCD8+ number and cytokine production in spleen cells. In conclusion, malathion and carbosulfan had significant immunomodulatory properties in the spleen with inflammation and oxidative stress induction in the liver.


PubMed | Laboratory of Aggression Physiology and Endocrine Metabolic Studies
Type: Journal Article | Journal: Iranian journal of basic medical sciences | Year: 2016

Lead (Pb) is a toxic metal inducing many destructive effects leading to a broad range of physiological, biochemical, and neurological dysfunctions in humans and laboratory animals.Here, we investigated the effect of chronic exposure to Pb (50 mg/l) on oxidative stress, hepatotoxicity, nephrotoxicity, and lipid profile of two different age groups of female rats treated with Pb from delivery until puberty period (40 days, Pb40) and post puberty period (65 days, Pb65).Our results clearly show that the administration of Pb produces oxidative damage in liver and kidney, as strongly suggested by the significant increase in TBARS, decrease in total SH, and the alteration of SOD activity. Elevation in liver function biomarkers, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and reduction in total protein (liver and plasma) and albumin are evidence of perturbations of liver synthetic function. In young Pb-treated group, Pb-induced nephropathy was more pronounced by the increase in the levels of creatinine, urea, and uric acid. However, hyperlipidemia was evident for both Pb-exposed groups leading to a potential risk for cardiovascular diseases and atherosclerosis.It is concluded that Pb induces metabolic and oxidative disturbances depending on the age of the animals, which are not negligible.

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