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The current investigation was carried out to estimate the protective effect of aqueous extract of Cheatomorpha gracilis (AEC) against High fat Diet (HFD) induced liver damage in mice. The results of the in vitro study showed that AEC have higher antioxidant capacities in the DPPH and hydroxyl radical-scavenging assays. Indeed, many phenolic compounds (gallic acid, quercetin, naringenin, apigenin, kaempferol and rutin) were identified in the AEC. In the animal studies, during 6 weeks, HFD promoted oxidative stress with a rise level of malonaldehyde (MDA), protein carbonyls (PCOs) levels and a significant decrease of the antioxidant enzyme activities such as superoxide dismutase, catalase and glutathione peroxidase. Interestingly, the treatment with AEC (250 mg/kg body weight) significantly reduced the effects of HFD disorders on some plasmatic liver biomarkers (AST, ALT and ALP) in addition to, plasmatic proteins inflammatory biomarkers (α2 and β1 decreases / β2 and γ globulins increases). It can be suggest that supplementation of MECG displays high potential to quench free radicals and attenuates high fat diet promoted liver oxidative stress and related disturbances.

The current study was carried out to estimate the protective effect of methanolic extract of Chaetomorpha gracilis (MECG) against High Cholesterol Diet (HCD) induced erythrocyte damage in mice. The results of the in vitro assay showed that MECG have higher antioxidant capacities in the DPPH, TAC, ABTS, NBT, NO . inhibition assays. The HPLC analysis confirmed that this potential antioxidant seems to be due to the active compounds, in particular polyphenols, flavonoids. HCD promoted oxidative stress with a rise the level of malonaldehyde (MDA), advanced oxidation protein product (AOPP) levels and a significant decrease of the Vitamin C content, as well the antioxidant enzyme activities such as superoxide dismutase and glutathione peroxidase. In addition, HCD treatment caused significant lipid profile disorders via increase the cholesterol, triglycerides and LDL levels and reduction HDL-Ch level. A statistically significant decrease of Mg 2+ and Ca 2+ ATPase activities accompanied with a severe damage in the erythrocytes structure and hematological parameters alterations were also noted in hypercholesterolemic mice. Pre-treatment with MECG significantly restored biochemical markers and pathological lesions. It can be suggest that supplementation of MECG displays high potential to quench free radicals and attenuates high cholesterol diet induced erythrocytes oxidative stress and related damages.

Nicotine mediates some of the injurious effects caused by consuming tobacco products. The aim of this work is to investigate the protective effects of Mentha spicata extract (ME) supplementation on the testis and brain of nicotine-induced oxidative damage rats. ME extract showed interesting hydrogen peroxide-scavenging activity. HPLC-DAD analysis of ME revealed the presence of nine compounds among them gallic acid was the major one (165.44 µg/g ME). Thirty-two rats were randomly divided into four groups: control, a nicotine-treated group (1 mg/kg i.p.), a group receiving ME (100 mg/kg), and a group receiving both ME (100 mg/kg) and nicotine (1 mg/kg). After 2 months of treatment, the in vivo results showed that nicotine exhibited an increase in the body, brain, testis and accessory sex organ weights, sperm count and sperm motility. In addition, exposure to nicotine significantly (p < 0.01) increased acetylcholinesterase level (AChE) in brain, lipid peroxidation level in brain and testis as compared to control group. The antioxidant enzymes results showed that nicotine treatment induced a significant decrease (p < 0.01) in brain and testis antioxidant enzymes such as catalase, superoxide dismutase and glutathione peroxidase as compared to control group. Interestingly, pretreatment with ME significantly (p < 0.01) restored the majority of these biological parameters to normal levels, as well as a histological improvement. Obtained results suggest that ME contains promising substances that counteract the nicotine-intoxication and can be efficient in the prevention of brain and testis toxicity complications.

High fat diet (HFD) exposure is associated with various pathological dysfunctions, including haematological disorders and oxidative stress. The in vitro analysis of AECG revealed the presence of important levels of polyphenols and flavonoids, and denoted antioxidant capacities confirmed by nitric oxide radical (NO • ), reducing the power and HPLC chemical components' determinations. The animals exposed to HFD revealed a severe damage in the blood cells structure and haematological parameters accompanied with a significant decrease in serum Mg 2+ and Ca 2+ ATPase activities. Furthermore, malondialdehyde (MDA) and the advanced oxidation of protein products (AOPP) levels were significantly increased, while vitamin C level, superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities were markedly reduced in the erythrocytes and platelets of HFD-treated mice. However, the co-administration of AECG with HFD-treated animals restored the parameters cited above to near-normal values. Therefore, our investigation revealed that Chaetomorpha gracilis extract was a useful element preventing HFD-induced blood cells damage.

Pesticides, such as organophosphorus and pyrethroids, are extensively used in the agrofields which can significantly increase crop productivity. Humans are exposed to pesticides via dermal contact, inhalation and ingestion due to occupational exposure. The objective of the present study was to evaluate the protective role of the aqueous extract of Crataegus oxyacantha during acute exposure of rats to the combination of deltamethrin (DM) and chlorpyrifos (CPF) in rats (DCF). The combination of vitamins C and E (Vit CE) was used as a standard antioxidant. The Crataegus oxyacantha extract revealed the presence of a high level of phenolic compounds identified by HPLC analysis. Male wistar rats were divided into six groups: (I) corn oil, (II) AECO (1 ml/100 g), (III) DCF (DM 5 mg/kg, CPF 1 mg/kg), (IV) AECO + DCF, (V) Vit CE (Vit C 100 mg/kg, Vit E 100 mg/kg), and (VI) Vit CE + DCF. AECO and Vit CE were administered 10 days before the administration of DCF. The findings revealed that the administration of DM and CPF mixture induced a significant decrease in serum AChE and DNA damage, as indicated by brain DNA fragmentation. In addition, behavioral tests by open field and elevated plus maze showed impaired recognition memory. The results showed that AECO or Vit CE alleviated significantly neurobehavioral alterations, reduced lipid peroxidation in brain, and restored the antioxidant parameters (SOD, CAT, GPx and GSH) to normal levels. Furthermore, brain DNA fragmentation and histopathology in DCF treated rats were improved by AECO administration. All results revealed that C. oxyacantha extract, rich in polyphenolic compounds, had potential antioxidant effects on the combination of DM and CPF-induced oxidative brain damage., (Copyright © 2019. Published by Elsevier Masson SAS.)

Previous studies have brought to light the toxic effect of cerium chloride (CeCl 3 ) but very little is known about the oxidative brain injury caused by this metal. Medical plants have a well-recognized role in the management of damage caused by pollutants such as CeCl 3 . Syzygium aromaticum, a potent natural source of bioactive compounds and rich in secondary metabolites, has a broad range of biological functions. The aim of this study is to investigate the capacity of Syzygium aromaticum ethanol extract (ESA) to improve the adverse effects of CeCl 3 in the brain tissue. Adult mice were exposed to CeCl 3 (20 mg/kg body weight [BW]), with or without ESA, for 60 days. We investigate mice's behavior, damages of cholinergic system and oxidative stress parameters in mice brain. In the present study, in vitro test confirmed that ESA has antioxidant capacity attributed to the presence of flavonoids, polyphenols, and tannins contents. In vivo study showed that CeCl 3 caused brain injuries manifested in memory impairment, increase in acetylcholinesterase activity, oxidative stress biomarkers (lipid, proteins, enzymatic and non-enzymatic antioxidant systems), and histopathological alteration in brain tissue. Addition of ESA repaired memory impairment, decreased acetylcholinesterase activity, restored oxidative state, and prevented histopathological alteration. In conclusion, the experimental results showed the protective effects of ethanol extract of Syzygium aromaticum against cerium-induced brain damage.

Cerium chloride (CeCl 3 ) is considered an environmental pollutant and a potent neurotoxic agent. Medicinal plants have many bioactive compounds that provide protection against damage caused by such pollutants. Curcuma longa is a bioactive compound-rich plant with very important antioxidant properties. To study the preventive and healing effects of Curcuma longa on cerium-damaged mouse brains, we intraperitoneally injected cerium chloride (CeCl 3 , 20 mg/kg BW) along with Curcuma longa extract, administrated by gavage (100 mg/kg BW), into mice for 60 days. We then examined mouse behavior, brain tissue damage, and brain oxidative stress parameters. Our results revealed a significant modification in the behavior of the CeCl 3 -treated mice. In addition, CeCl 3 induced a significant increment in lipid peroxidation, carbonyl protein (PCO), and advanced oxidation protein product levels, as well as a significant reduction in superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities. Acetylcholinesterase (AChE) activity remarkably increased in the brain of CeCl 3 -treated mice. Histopathological observations confirmed these results. Curcuma longa attenuated CeCl 3 -induced oxidative stress and increased the activities of antioxidant enzymes. It also decreased AChE activity in the CeCl 3 -damaged mouse brain that was confirmed by histopathology. In conclusion, this study suggests that Curcuma longa has a neuroprotective effect against CeCl 3 -induced damage in the brain.

Euphorbia paralias is known in traditional medicine as an anti-inflammatory agent, a purgative and for its local anesthetic property. To the best our knowledge, renal toxicity of this substance has not been previously reported. In this paper, we report the case of a 29-year-old male who developed renal damage following ingestion of Euphorbia paralias. He had been on follow-up for nephrotic syndrome since 1986, although irregularly, with several relapses but each responding well to steroid therapy. A kidney biopsy had not been performed earlier due to refusal by the patient. He was off steroids since April 2008 because the patient developed osteoporosis. He was admitted with general malaise and oliguria to our department in May 2009, following repeated vomiting and watery diarrhea for three days. On examination, he was edematous but had normal vital signs except for a pulse rate of 120/min. Hemoglobin was only 5.5 g/dL but with normal white cell and platelet counts. Blood biochemistry showed evidence of advanced renal failure with a serum creatinine level of 1835 μmol/L and urea at 44.6 mmol/L, sodium of 132 μmol/L and potassium at 4.3 mmol/L. He had features of nephrotic syndrome with severe hypoproteinamia and 24-h urinary protein of 10.45 g. Ultrasonography revealed enlarged kidneys with a reduced echogenecity of the medulla and the papillae. Subsequently, after hemodialysis with blood transfusion, a kidney biopsy was performed that showed focal segmental glomerulosclerosis associated with an acute tubular injury. On intensive interrogation, the patient gave a history of ingesting boiled Euphorbia paralias as a native treatment for edema, ten days prior to the onset of the current illness. A diagnosis of acute renal failure (ARF) resulting from the possible nephrotoxic effect of Euphorbia paralias poisoning was made. He was treated with intermittent hemodialysis and corticosteroids. Serum creatinine values improved after 48 days. At six months following the intoxication, serum creatinine of the patient was 240 μmol/L. In cases of unexplained ARF, a toxic mechanism should always be considered and acute renal failure caused by Euphorbia paralias should be included as a cause if renal toxicity is suspected in those places where it is being used as a native medicine.