RESUMEN
The current study explored the efficacy of piperine in attenuating arsenic induced high fat diet aggravated oxidative stress mediated injury in hepatic and cardiac tissues of male Wistar rats. Oral administration of piperine significantly (p < 0.05) reduced the levels of organ specific and oxidative stress biomarkers in arsenic and high fat diet treated rat hepatic and cardiac tissues in a dose dependant manner with the dose of 60 mg/kg b.w. exhibiting maximum protection. Arsenic induced high fat diet aggravated oxidative stress mediated damages in liver and heart tissues led to decreased activities of antioxidant enzymes, ROS generation, diminished activities of Krebs' cycle and respiratory chain enzymes, collapsed mitochondrial membrane potential, mitochondrial DNA damage along with altered lipid metabolism and inflammatory cytokine levels. Histochemical and histopathological studies supported the above findings. Piperine efficiently counteracted the arsenic induced high fat diet aggravated oxidative stress mediated damages by modulating antioxidant defense mechanism along with free radical quenching ability. These findings indicate that piperine protected the arsenic induced high fat diet aggravated hepatic and cardiac injuries which underline the importance of piperine in providing a possible therapeutic regime for the amelioration of arsenic-induced high fat diet aggravated oxidative stress mediated organ damages.
Asunto(s)
Alcaloides/farmacología , Antioxidantes/farmacología , Arsénico/toxicidad , Benzodioxoles/farmacología , Dieta Alta en Grasa , Lesiones Cardíacas/etiología , Hígado/lesiones , Estrés Oxidativo/efectos de los fármacos , Piperidinas/farmacología , Alcamidas Poliinsaturadas/farmacología , Animales , Lesiones Cardíacas/metabolismo , Hígado/metabolismo , Masculino , Ratas , Ratas Wistar , Especies Reactivas de Oxígeno/metabolismoRESUMEN
Arsenic is a well known global groundwater contaminant. Exposure of human body to arsenic causes various hazardous effects via oxidative stress. Nutrition is an important susceptible factor which can affect arsenic toxicity by several plausible mechanisms. Development of modern civilization led to alteration in the lifestyle as well as food habits of the people both in urban and rural areas which led to increased use of junk food containing high level of fat. The present study was aimed at investigating the effect of high fat diet on heart and liver tissues of rats when they were co-treated with arsenic. This study was established by elucidating heart weight to body weight ratio as well as analysis of the various functional markers, oxidative stress biomarkers and also the activity of the antioxidant enzymes. Histological analysis confirmed the biochemical investigations. From this study it can be concluded that high fat diet increased arsenic induced oxidative stress.
Asunto(s)
Arsénico/toxicidad , Dieta Alta en Grasa , Corazón/efectos de los fármacos , Hígado/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Animales , Peso Corporal/efectos de los fármacos , Relación Dosis-Respuesta a Droga , Pruebas de Función Cardíaca , Pruebas de Función Hepática , Masculino , Tamaño de los Órganos/efectos de los fármacos , Ratas , Ratas WistarRESUMEN
The present study was undertaken to explore the protective effect of melatonin against isoproterenol bitartrate (ISO)-induced rat myocardial injury and to test whether melatonin has a role in preventing myocardial injury and recovery when the ISO-induced stress is withdrawn. Treatment for rats with ISO altered the activities of some of the key mitochondrial enzymes related to energy metabolism, the levels of some stress proteins, and the proteins related to apoptosis. These changes were found to be ameliorated when the animals were pretreated with melatonin at a dose of 10 mg/kg BW, i.p. In addition to its ability to reduce ISO-induced mitochondrial dysfunction, we also studied the role of melatonin in the recovery of the cardiac tissue after ISO-induced damage. Continuation of melatonin treatment in rats after the withdrawal of ISO treatment was found to reduce the activities of cardiac injury biomarkers including serum glutamate oxaloacetate transaminase (SGOT), lactate dehydrogenase (LDH), and cardio-specific LDH1 to control levels. The levels of tissue lipid peroxidation and reduced glutathione were also brought back to that seen in control animals by continued melatonin treatment. Continuation of melatonin treatment in post-ISO treatment period was also found to improve cardiac tissue morphology and heart function. Thus, the findings indicate melatonin's ability to provide cardio protection at a low pharmacological dose and its role in the recovery process. Melatonin, a molecule with very low or no toxicity may be considered as a therapeutic for the treatment for ischemic heart disease.
Asunto(s)
Isoproterenol/toxicidad , Melatonina/uso terapéutico , Mitocondrias Cardíacas/enzimología , Isquemia Miocárdica/metabolismo , Miocardio/metabolismo , Animales , Antioxidantes/metabolismo , Apoptosis/efectos de los fármacos , Aspartato Aminotransferasas/sangre , Glutatión/metabolismo , Isoenzimas/metabolismo , L-Lactato Deshidrogenasa/sangre , L-Lactato Deshidrogenasa/metabolismo , Peroxidación de Lípido , Peróxidos Lipídicos/metabolismo , Masculino , Mitocondrias Cardíacas/efectos de los fármacos , Isquemia Miocárdica/sangre , Isquemia Miocárdica/inducido químicamente , Isquemia Miocárdica/enzimología , Ratas , Ratas Sprague-DawleyRESUMEN
Necrotizing fasciitis is most often associated with bacterial infections. Zygomycosis is an uncommon infection causing necrotizing fasciitis. We report 18 such cases of zygomycotic necrotizing fasciitis, of these, 15 were immunocompetent. Of the eight cases cultured, five were positive for Apophysomyces elegans. A retrospective case review conducted at a tertiary referral center, from 1998 to 2004, 18 cases of fungal necrotizing fasciitis were diagnosed based on histomorphology of fungal organisms; and in few of the cases diagnosis was supported by mycologic culture reports. Of the total of 18 cases, culture report was available in eight cases, and out of which five of them grew A. elegans. Fifteen patients were immunocompetent. Clinical presentation, mycologic findings and histopathologic results were evaluated. A review of the literature pertaining to A. elegans infection was also done. Histopathologic examination showed broad, predominantly aseptate and occasional pauciseptate, thin-walled fungal hyphae with occasional angioinvasion. To the best of our knowledge, this is the first largest series of zygomycotic necrotizing fasciitis from India. Herein, we present data on 18 cases of necrotizing fasciitis assosiated with zygomycosis. Most of the cases in our series were immunocompetent. Nonsuppurative necrosis with presence of typical fungal profiles was important histologic feature. Zygomycosis must be considered in the differential diagnosis not only in immunocompromised patients but also in the absence of any underlying disorders.