Several anticancer agents currently used in clinical settings are derived from plants, such as vinblastine vincristine fromCatharanthus roseus, and paclitaxel fromTaxus brevifolia. In this context, the present study investigates the acute and subchronic toxicity ofBerberis hispanica, a medicinal plant traditionally used in North Africa, particularly in the Tikjda region, for its therapeutic properties. The aim was to assess its potential toxic effects on liver and kidney function in Musfemalemusculusmice. The aqueous extract was prepared from the dried root bark through maceration in water, followed by filtration and concentration.cewereMi randomly divided into groups and received daily oral doses of 0, 75, 375, 750, or 1500 mg/kg of extract for six weeks. Acutexiciytowas evaluated based on behavioral changes and mortality within 24 hours. Subchronic toxicity was assessed through biochemicalsesofanaly serum liver enzymes (alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase) and renal markers (urea,inine,creat albumin), as well as histopathological examination of liver and kidney tissues. No mortality or significant behavioral changeswere observed following acute administration. Subchronic exposure to the highest dose (1500 mg/kg) resulted in a 33 % mortalityand rate mild histological alterations. Biochemical markers showed limited variations compared to controls, suggesting a low levelofpatrenalhe toxicity. These findings indicate that the aqueous extractofBerberis hispanica exhibits low acute and subchronic toxicity in mice, supporting its potential for therapeutic use, pending further pharmacological and toxicological evaluation.

Cardiometabolic disorders, including hepatic steatosis, insulin resistance, and cardiovascular diseases, represent major public health challenges, frequently associated with Western diets high in fats, carbohydrates, and proteins. Dietaryyphenols, pol particularly those found in apples, have shown promising protective effects against metabolic and cardiovascular dysfunctions.This study investigated the therapeutic potential of apple juice in female Wistar rats subjected to a diet-induced model ofmetabolic syndrome. The animals were randomly divided into three groups: a control group (C) fed a standard chow diet; a group fed a high-carbohydrte, high-fat, and high-protein diet (HCHFP; 60 % fat, 30 % carbohydrates, and 9 % protein) for eight weeks; and a third groupP+ (HCHFA) receiving the same diet, supplemented orally with fresh apple juiceMalus (domestica) (15 mL/kg/day) during the final 30 days of the experimental period. Biochemical parameters were assessed in plasma and tissues to evaluate lipid and glucose metabolism,tiveoxida stress (MDA, AOPP, SOD, CAT), inflammatory markers (NO, MCP-1, TNF-alpha), and metabolic regulators (AMPK). Histological examinations of hepatic and cardiac tissues were also performed. Apple juice supplementation significantly improved lipidlycemicandg profiles, enhanced antioxidant enzyme activities, reduced inflammation, and alleviated hepatic steatosis and myocardialThese damage. findings highlight the potential of apple juice as a functional nutritional intervention with antioxidant, anti-inflammatorynd, metabolic regulatory properties against diet-induced cardiometabolic disorders.

Endocrine disruptors (ED) are designed by the WHO as “Any chemical substance foreign to the body that can interfere with the functioning of an endocrine system and induce deleterious effects on the latter with a transgenerational effect”. These compounds are present in our environment, carried by air, water, soil and their toxicity is proven because they interact with the hormones synthesis, degradation, transport and mode of action. Exposure of humans and animals to ED through food and/or domestic use is currently a hot topic. The results of numerous independent studies have highlighted the carcinogenic effect of ED, particularly in the case of hormone-dependent cancers. These results provide from experimental and clinical studies. By modifying hormonal function, these compounds have potentially patho-logical consequences for the organism exposed to them or for its descendants. They act by binding to receptors or enzymes and modulate, through their agonist or antagonist activity, the effectiveness or metabolism of natural hormones. The majority of ED are estrogens low-activity. Some are also anti-androgens and/or interfere with the activity of thyroid hormones. ED pose difficult problems, especially since their nature varies over time. Some have been banned, but others persist and concentrate via the food chain in adipose tissue, and cause delayed and multiple effects on human health. Some are toxic for the reproductive function in men via a drop in sperm concentration, others are neurotoxic (Parkinson disease, behavioral disorders) but also those involved in the increasing incidence of chronic diseases, such as type 2 diabetes, obesity and certain hormone-sensitive cancers. Only the cocarcinogenic risk of ED will be discussed in this review, after the presentation of the different families of ED (industrial products in food, food additives, industrial products in packaging, pesticides, substances of natural origin). [Les perturbateurs endocriniens (PE) sont définis par l'OMS comme « toute substance chimique étrangère à l'organisme pouvant interférer avec le fonctionnement d'un système endocrinien et induire des effets délétères sur ce dernier avec un effet transgénérationnel ». Ces composés sont présents dans notre environnement, véhiculés par l’air, l’eau, le sol et leur toxicité est avérée car ils interagissent avec la synthèse, la dégradation, le transport et le mode d’action des hormones. L’exposition des humains et des animaux aux PE par voie alimentaire et/ou domestique est à ce jour un sujet d’actualité. Les résultats de nombreuses études indépendantes ont mis en exergue l’effet cancérigène des PE, notamment dans le cas de cancers hormono-dépendants. Ces résultats proviennent d’études expérimentales et cliniques. Ces composés, en modifiant une fonction hormonale, ont potentiellement des conséquences pathologiques pour l’organisme qui y est exposé ou pour sa descendance. Ils agissent en se liant à des récepteurs ou à des enzymes et modulent, par leur activité agoniste ou antagoniste, l’efficacité ou le métabolisme d’hormones naturelles. La majorité des PE sont des oestrogènes de faible activité. Certains sont également des anti-androgènes et/ou interfèrent avec l’activité des hormones thyroïdiennes. Les PE posent des problèmes difficiles d’autant que leur nature varie dans le temps. Certains ont été interdits, mais d’autres persistent et se concentrent via la chaine alimentaire dans le tissu adipeux et entrainent des effets retardés et multiples sur la santé humaine. Certains sont toxiques pour la fonction de reproduction chez l’homme via une baisse de la concentration de spermatozoïdes, d’autres sont neurotoxiques (maladie de Parkinson, troubles du 32 comportement) mais aussi sont retrouvés ceux impliqués dans l’incidence croissante de maladies chroniques, tels que le diabète de type 2, l’obésité et certains cancers sensibles aux hormones. Ne sera évoqué dans cette revue que le risque cocarcinogène des PE, après la présentation des différentes familles de PE (produits industriels dans les aliments, additifs alimentaires, produits industriels dans les emballages, pesticides, substances d’origine naturelle).]

Obesity -related pathophysiologies such as insulin resistance and the metabolic syndrome show a markedly increased risk for type 2 diabetes and atherosclerotic cardiovascular disease. This risk appears to be linked to alterations in adipose tissue function, leading to chronic inflammation and the dysregulation of adipocyte-derived factors. Brassica rapa have been used in traditional medicine for the treatment of several diseases, including diabetes.. This study aimed to investigate the effect of nutritional stress induced by a high -fat and high -sucrose diet on the pathophysiology of visceral adipose tissue and the therapeutic effect of Brassica rapa in male Wistar rats. We subjected experimental rats to a high -fat (10 %) high -sucrose (20 %)/per day for 11 months and treated them for 20 days with aqueous extract Br (AEBr) at 200 mg/kg at the end of the experiment. At the time of sacrifice, we monitored plasma and tissue biochemical parameters as well as the morpho-histopathology of visceral adipose tissue. We found AEBr corrected metabolic parameters and inflammatory markers in homogenized visceral adipose tissue and reduced hypertrophy, hyperplasia, and lipid droplets. These results suggest that AEBr enhances anti -diabetic, anti-inflammatory and a protective effect on adipose tissue morphology in type 2 diabetes and obesity.

Endocrine disruptors (ED) are designed by the WHO as “Any chemical substance foreign to the body that can interfere with the functioning of an endocrine system and induce deleterious effects on the latter with a transgenerational effect”. These compounds are present in our environment, carried by air, water, soil and their toxicity is proven because they interact with the hormones synthesis, degradation, transport and mode of action. Exposure of humans and animals to ED through food and/or domestic use is currently a hot topic. The results of numerous independent studies have highlighted the carcinogenic effect of ED, particularly in the case of hormone-dependent cancers. These results provide from experimental and clinical studies. By modifying hormonal function, these compounds have potentially patho-logical consequences for the organism exposed to them or for its descendants. They act by binding to receptors or enzymes and modulate, through their agonist or antagonist activity, the effectiveness or metabolism of natural hormones. The majority of ED are estrogens low-activity. Some are also anti-androgens and/or interfere with the activity of thyroid hormones. ED pose difficult problems, especially since their nature varies over time. Some have been banned, but others persist and concentrate via the food chain in adipose tissue, and cause delayed and multiple effects on human health. Some are toxic for the reproductive function in men via a drop in sperm concentration, others are neurotoxic (Parkinson disease, behavioral disorders) but also those involved in the increasing incidence of chronic diseases, such as type 2 diabetes, obesity and certain hormone-sensitive cancers. Only the cocarcinogenic risk of ED will be discussed in this review, after the presentation of the different families of ED (industrial products in food, food additives, industrial products in packaging, pesticides, substances of natural origin). [Les perturbateurs endocriniens (PE) sont définis par l'OMS comme « toute substance chimique étrangère à l'organisme pouvant interférer avec le fonctionnement d'un système endocrinien et induire des effets délétères sur ce dernier avec un effet transgénérationnel ». Ces composés sont présents dans notre environnement, véhiculés par l’air, l’eau, le sol et leur toxicité est avérée car ils interagissent avec la synthèse, la dégradation, le transport et le mode d’action des hormones. L’exposition des humains et des animaux aux PE par voie alimentaire et/ou domestique est à ce jour un sujet d’actualité. Les résultats de nombreuses études indépendantes ont mis en exergue l’effet cancérigène des PE, notamment dans le cas de cancers hormono-dépendants. Ces résultats proviennent d’études expérimentales et cliniques. Ces composés, en modifiant une fonction hormonale, ont potentiellement des conséquences pathologiques pour l’organisme qui y est exposé ou pour sa descendance. Ils agissent en se liant à des récepteurs ou à des enzymes et modulent, par leur activité agoniste ou antagoniste, l’efficacité ou le métabolisme d’hormones naturelles. La majorité des PE sont des oestrogènes de faible activité. Certains sont également des anti-androgènes et/ou interfèrent avec l’activité des hormones thyroïdiennes. Les PE posent des problèmes difficiles d’autant que leur nature varie dans le temps. Certains ont été interdits, mais d’autres persistent et se concentrent via la chaine alimentaire dans le tissu adipeux et entrainent des effets retardés et multiples sur la santé humaine. Certains sont toxiques pour la fonction de reproduction chez l’homme via une baisse de la concentration de spermatozoïdes, d’autres sont neurotoxiques (maladie de Parkinson, troubles du comportement) mais aussi sont retrouvés ceux impliqués dans l’incidence croissante de maladies chroniques, tels que le diabète de type 2, l’obésité et certains cancers sensibles aux hormones. Ne sera évoqué dans cette revue que le risque cocarcinogène des PE, après la présentation des différentes familles de PE (produits industriels dans les aliments, additifs alimentaires, produits industriels dans les emballages, pesticides, substances d’origine naturelle).]

Resveratrol (RES) and quercetine (QRC), is a promising agent relevant for both cancer chemoprevention and treatment via several signaling pathways, involved in their anticancer activity related to its chemotherapeutic potental,cited assowith the induction of ROS generation in cancer cells, leading to apoptosis. In our study, we have summarized the mechanismsn of of actio RES and QRC, and their pharmacological implications and potential therapeutic applications in cancer therapy. After f treatmentHep o 2 cells with QRC or RES, the death pathways such as the cytochrome c release, ERK1/2 and IRS-1 pathways were upregulated, while cell survival pathway, including PI3K/AKT were downregulated. The RES and QRC caused oncosis, cells hypertrophy, hypercondensatin of chromatin, rupture of the plasma membrane and nuclear membrane, and formation of apoptotic bodies. Morphometric measurements of some cellular and nuclear parameters showed that RES and QRC induced an increase in cells and nuclear size, the nucleocytoplasmic ratio remained below 1 (N-Cyt R < 1), sign of low nuclear activity. The RES and QRC induced apoptosis of Hep2 cells by increasing of oxidative stress markers, MDA, and by modulating detoxifying enzymes, CAT and SOD. Our study results prove antiproliferatived an proapoptotic properties of quercetin and resveratrol with regard to larynx cancer.

It has been previously shown that clinical cardiovascular manifestations can be caused by mild changes in thyroid function. However, the implication of angiotensinogen ( Agt ) and vascular smooth muscle cells (VSMCs) dysfunction in the pathophysiology of cardiovascular manifestations in hypothyroidism have not yet been investigated. We induced experimental hypothyroidism in Psammomys obesus by administering carbimazole for five months. At the end of the experiment, the animals were sacrificed and histopathological analysis was performed using Masson's trichrome staining of the aorta and thyroid gland. The expression of the Agt gene and the genes implicated in cholesterol metabolism regulation in the liver and VSMCs was determined by qRT-PCR. Histological observations revealed profound remodeling of the aorta structure in animals with hypothyroidism. In addition, Agt gene expression in the liver was significantly increased. In vitro study, showed that VSMCs from hypothyroid animals overexpressed 3-hydroxy-3-methylglutaryl coenzyme A reductase ( Hmgcr ) and Acyl CoA:cholesterol acyltransferase ( Acat ) 1, with failure to increase the efflux pathway genes (ATP-binding cassette subfamily G member ( Abcg) 1 and 4 ). These results suggest that hypothyroidism leads to vascular alterations, including structural remodeling, VSMCs cholesterol metabolism dysfunction, and their switch to a synthetic phenotype, together with hepatic Agt gene overexpression.

Abstract Thyroid hormones (TH) have several effects on the cardiovascular system. A slight decline in TH levels has harmful effects on the vascular system. The current study aimed to investigate whether a decrease in TH plasma levels was responsible for the expression of some atherosclerosis markers. Experimental hypothyroidism was induced in Psammomys obesus by administering 0.03% carbimazole in their drinking water for five months (M5). The animals were sacrificed at M5, and histopathological analysis of the thoracic aorta and thyroid gland was performed after Masson's trichrome staining. The expression of the angiotensinogen (Agt) gene and the genes implicated in cholesterol metabolism regulation in the liver and vascular smooth muscle cells (VSMCs) was determined by qRT-PCR. Finally, we assessed the in vitro proliferation rate of VSMCs derived from the aortas of the two groups of animals. Hypothyroidism was associated with increased expression of Agt in the liver and 3-hydroxy-3-methylglutaryl coenzyme A reductase (Hmgcr) and Acyl CoA:cholesterol acyltransferase (Acat) 1 genes (cholesterol synthesis and esterification pathway) in VSMCs, with failure to increase efflux pathway genes (ATP-binding cassette subfamily G member (Abcg) 1 and 4) in these vascular cells. Moreover, reduction in TH induces aortic endothelial cell and subendothelium hypertrophy, and disorganization of the media with rupture of the elastic fiber network. All these results suggest that hypothyroidism can lead to atherosclerosis through the alteration of the physiology of VSMCs, mainly the phenotype switch and gene expression modification involved in the regulation of cholesterol metabolism.

BACKGROUND:Lipotoxicity is characterized by a metabolic disturbance leading to the development of nonalcoholic fatty liver disease (NAFLD). Some medicinal plant extracts exert hepatoprotective activity by modulating oxidative stress, inflammation, and metabolic disorders. Scolymus hispanicus or the golden thistle can be considered an important natural source of antioxidants. In traditional medicine, the consumption of this plant is recommended for diseases of the liver and intestines.OBJECTIVE:In this study, we aimed to determine the effects of Scolymus hispanicus on a hyperfatty diet- (HFD-) induced metabolic disorders, oxidative stress, and inflammation.MATERIALS AND METHODS:Our experiment focused on the administration of an HFD (40%) in Rattus norvegicus for 2 months and treatment with the aqueous extract of Scolymus hispanicus at a rate of 100 mg/kg during the last eight days of experimentation. In this context, several aspects were studied: the evaluation of blood biochemical parameters, liver function such as lipids and glycogen, markers of oxidative stress (TBARS, carbonyl proteins, advanced oxidation proteins, catalase, and SOD) and inflammation (NO and NFkB), morphological study of hepatocytes in primary culture, and histological study of the liver.RESULTS:Lipotoxicity induced metabolic disorders, both serum and tissue. HFD induced an increase in the total lipids and a decrease in glycogen reserve and an alteration in the oxidant-antioxidant balance. HFD induced an increase in markers of liver damage, which resulted in NAFLD, confirmed by histological study and hepatocytes cell culture. Scolymus appears to have lipid-lowering, hypoglycemic, anti-inflammatory and antioxidant properties. It improved glucose tolerance and the condition of fatty liver disease.CONCLUSION:Golden thistle improves glucose tolerance and hyperlipidemia and ameliorates hepatic steatosis by reducing oxidative stress, inflammation, and lipid accumulation. Its incorporation into a dietary program or as an aliment supplement would prevent hepatic complications associated with an HFD.

In our study, we propose to analyze the effects of resveratrol (RES) and quercetin (QRC) on proliferation markers, oxidative stress, apoptosis, and inflammation of aortic fibroblasts of Psammomys obesus after induced oxidative stress by hydrogen peroxide (H2O2). Fibroblasts were incubated in RES 375 μM and QRC 0.083 μM for 24 hours after exposure to H2O2 1.2 mM for 6 hours. We performed the proliferation rate, cells viability, morphological analyses, cytochrome c, Akt, ERK1/2, and p38 MAPK quantification. The redox status was achieved by proportioning of malondialdehyde, nitric monoxide, advanced oxidation protein products, carbonyl proteins, catalase, and superoxide dismutase activity. The inflammation was measured by TNFα, MCP1, and NF-kB assay. The extracellular matrix (ECM) remodeling was performed by SDS-PAGE. Stressed fibroblasts showed a decrease of cell proliferation and viability, hypertrophy and oncosis, chromatin hypercondensation and increase of cytochrome c release characteristic of apoptosis, activation of ERK1/2 and Akt pathway, and decreases in p38 MAPK pathways marking the cellular resistance. The redox state was disrupted by increased malondialdehyde, nitric monoxide, advanced oxidation protein products, carbonyl protein production, catalase and superoxide dismutase activity, and a decreased production of proteins including collagens. Inflammation state was marked by MCP-1, TNFα, and NF-kB increase. Treatment of fibroblasts stressed by RES and QRC inverted the oxidative stress situation decreasing apoptosis and inflammation, and improving the altered redox status and rearrangement of disorders observed in extracellular matrix. H2O2 induced biochemical and morphological alterations leading to apoptosis. An improved general condition is observed after treatment with RES and QRC; this explains the antioxidant and antiapoptotic effects of polyphenols.

This study was made to investigate the effect of a diet rich in fat and sucrose and therapeutic involvement of aqueous extract of Brassica rapa (Br). Diabetic rats were submitted to a natural diet supplemented in high fat (10%) high sucrose (20%)/per day for 9 months. After this period, we have administered the treatment with aqueous extract of Br via oral gavage at 200 mg/kg during 20 days. The biochemical parameters were measured in the plasma and the inflammatory-oxidative stress markers were measured in the supernatant of aorta and heart tissues. The results showed that Br extract reduced the metabolic disorders, the inflammatory and oxidative markers in plasma and homogenate tissue of rats. These results suggested that the aqueous extract of Br enhanced the anti-diabetic. anti-inflammatory and antioxidant defense against reactive oxygen species produced under type 2 diabetes and hyper-insulinemic conditions.

Introduction: Insulin resistance marked by an inflammatory response via production TNF α and compensatory hyperinsulinemia leading to long term installation of glucolipotoxicity and type 2 diabetes. Material and Methods : In this study, we analyzed the effect of polyphenol exracts Globularia alypum (Ga) in vitro, following an induced stress on the cardiomyocyte of Rattus norvegicus by the addition of a high dose of insulin (10 UI/ml). In this case, we evaluated the proliferation rate by counting and evaluated the cellular content on nitric oxide (NO), malondialdehyde (MDA) and catalase. Results and Discussion: In the presence of high dose of insulin, cardiomyocytes showed deceased cell survival, an imbalance of redox status in favor of increase of NO and MDA and decrease of an enzyme of the antioxidant system, catalase. Following the action of Ga polyphenol extracts, we recorded an improvement in the rate of cell proliferation, decreased levels of NO and MDA and increased levels of catalase activity. Conclusion: the state of stress induced insulin resistance mimed by the high dose of insulin of cardiomyocytes marked by physiological and biochemical alterations. These, apoptosis precursors are attenuated after addition of polyphenol exracts Globularia alypum which may be a therapeutic target upstream on the installation of T2DM.

Context. Brassica rapa is considered as natural source of antioxidants and is used to treat diabetes. Objective. Our study carried the impact of glucotoxicity induced in vivo and in vitro in vascular smooth muscle cells (VSMCs) in Psammomys and the therapeutic effect of Brassica rapa (AEBr). Materials and Methods. We administered a hyperglucidic diet (30% sucrose) for 9 months and a treatment for 20 days with AEBr at 100 mg/kg. VSMCs were submitted to D-Glucose (0.6%) for 48 hours and treated with AEBr (2100 μg/mL) for 24 hours. We measured, in blood metabolic parameters, the redox statues and inflammatory markers in adipose tissue. Histological study was effectuated in liver. In VSMCs, we measured markers of glucotoxicity (IRS1p Serine, AKT) inflammation (NO, MCP1, TNFα, and NF-κB) and oxidative stress (oxidants and antioxydants markers). Cell viability and apoptosis were estimated by the morphological study. Results. AEBr corrects the metabolic parameters and inflammatory and oxidative markers in blood and homogenate tissue and reduces lipid droplets in liver. It induces, in VSMCs, a significant decrease of IRS1p serine, cyt c, NO, MCP1, TNFα, NF-κB, protein, and lipid oxidation and increases cell viability, AKT, ERK1/2, catalase, and SOD activity. Conclusion. Brassica enhanced the antidiabetic, anti-inflammatory, and antioxidant defense leading to the protection of cardiovascular diseases.

It was established that the sand rat Psammomys obesus is an experimental model of type diabetes 2 and dyslipidemia, in this in vivo study the sand rats were submitted to natural diet associated with fat (10%) and sucrose (20%) enriched diet /rat per day for 6 months.The initial time and once of the months, plasma parameters were evaluated and at 6 th month aortic morphology were examined.To simulate hyperinsulinemic stress, the effects of high dose of insulin 10 UI/ml during 6 h were investigated on subcultured aortic control fibroblasts which were implicated in extracellular matrix remodeling during the atherosclerosis process.In this work report, the proliferation rates, morphological aspects of apoptosis, few markers of oxidative stress (malonaldehyde and nitric oxid) and type I and III collagen contained in extracellular compartment were evaluated.Others animals received a high fat high sucrose diet showed hyperglycemia associated with hyperinsulinemia, dyslipidemia, hyperproteinemia, increase of cardiac markers, low and very low density lipoproteins and decrease high density lipoprotein versus control group.The aortas of diabetic ranimals were exhibited an important disorganization and remodeling of vascular extracellular matrix.In vitro results indicated a decrease in cellular proliferation rate, the apparition of some morphological characters of apoptosis (hypertrophy fibroblasts, hypercondensation chromatin, oncosis) and increase of malonaldehyde, total nitrite production in intracellular compartment and increase of total proteins, type I and III collagen especially type III were observed in extracellular compartment.The high fat high sucrose diet induced diabetes associated with hyperinsulinemia and development of extracellular matrix remodeling in sand rats similar to human advanced atherosclerotic lesions.The high insulin dose induced an increase of both some markers of oxidative stress caused apoptosis and extracellular type III collagen especially.

Objective: Chronic hyperglycemia characteristic of type diabetes 2 is responsible for the accelerated atherosclerosis with increased cardiovascular risk. In this study, we will propose to analyze the effect of a long-term of glucotoxicity in vivo in Psammomys obesus by addition of sucrose to 30% for 11 months and in vitro study of adventitial fibroblasts in the presence of D-glucose 0.6% for 7 days. Materials and methods: Evaluation of plasma biochemical parameters was carried out at the initial time and at the end of experiment. At autopsy, a morphological study of the aorta was performed after fixation in aqueous Bouin and staining with Masson’s trichrome. The experimental glucotoxicity is induced by incubation of fibroblasts in DMEM enriched with D-glucose at 0.6% for 7 days. The impact of glucotoxicity is assessed in the intracellular compartments through dosage of total nitrite and malondialdehyde, a product of lipid peroxidation, and thanks to a morphological assay after fixation of cells with aqueous bouin and blood staining with May Grünwald Giemsa. The evaluation of cell proliferation is accomplished by cell counting. Collagens I and III of the extracellular compartment are characterized by SDS-PAGE. Results: Animals subjected to sucrose showed hyperglycemia associated with hyperinsulinemia, dyslipidemia, hyperproteinemia, increased CPK and VLDL-LDL and decreased HDL. Histology of aortas revealed endothelial cells hypertrophy, severe disorganization of intima and media. In the presence of glucose, the proliferation of fibroblasts increases very significantly (P = 2.34 × 10-5), the rate of malonaldehyde, nitrite and total density of chains α2 (I) and α1 (I + III) extra-cellular collagens I and III increased significantly. After staining, the cells showed hypertrophy, vacuolation of cytoplasm and chromatin condensation with nuclear fragmentation, indicative of apoptosis. Conclusion: The glucotoxicity induced in vivo and in vitro is responsible for major structural and metabolic alterations leading to the acceleration of the atherosclerotic process.