Proteins but not Nucleic Acids are Molecular Targets for the Free Radical Attack During Reoxygenation of Rat Hepatocytes

Caraceni, Paolo; Maria, Nicola De; Ryu, H.S; Colantoni, Alessandra; Roberts, L. Jackson; Maidt, M.L.; Pye, Quentin N.; Bernardi, Mauro; Thiel, David H. Van; Floyd, Robert A.

doi:10.1016/s0891-5849(96)00571-0

Cited by 39 publications

(24 citation statements)

References 20 publications

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“…DNA was digested by incubation with DNAase I, endonuclease, and alkaline phosphatase (Schneider et al 1993). The amount of 8-OH-dG was measured by high-performance liquid chromatography (HPLC) with electrochemical detection as described previously (Floyd et al 1986;Caraceni et al 1997). …”

Section: Lmn Assaymentioning

confidence: 99%

Eicosapentaenoic acid protects against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced hepatic toxicity in cultured rat hepatocytes

et al. 2011

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2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a persistent and ubiquitous environmental contaminant. The health impact of TCDD exposure is of great concern to the general public. Recent reports have implied that eicosapentaenoic acid (EPA) might be a potential chemopreventive agent and influence hepatotoxicity. The aim of the current study was to explore the effectiveness of EPA in alleviating the toxicity of TCDD on primary cultured rat hepatocytes. EPA (5, 10 and 20 lM) was added to cultures alone or simultaneously with TCDD (5 and 10 lM). Rat hepatocytes were treated with TCDD and EPA for 48 h, and then cytotoxicity was detected by [3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide] (MTT) assay and lactate dehydrogenase (LDH) release, while total antioxidant capacity (TAC) and total oxidative stress (TOS) levels were determined to evaluate the oxidative injury. The DNA damage was also analyzed by liver micronucleus assay (LMN) and 8-oxo-2-deoxyguanosine (8-OH-dG). The results of MTT and LDH assays showed that TCDD but not EPA decreased cell viability. TCDD also increased TOS level and significantly decreased TAC level in rat hepatocytes in a clear dose dependent manner. On the basis of increasing doses, the dioxin caused significant increases of micronucleated hepatocytes (MNHEPs) and 8-OH-dG as compared to control culture. Whereas, in cultures treated with EPA alone, TOS level did not change and the level of TAC significantly increased. The presence of EPA with TCDD minimized the toxic effects of the dioxin on primary hepatocytes cultures. Noteworthy, EPA has a protective effect against TCDD-mediated DNA damages.

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Section: Lmn Assaymentioning

confidence: 99%

Eicosapentaenoic acid protects against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced hepatic toxicity in cultured rat hepatocytes

et al. 2011

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“…It has been demonstrated that inclusion of feed ingredients containing tannins resulted in undesirable physiological and biochemical effects (Armstrong et al, 1974;Smulikowska et al, 2001) including growth inhibition, negative nitrogen balances, reduced intestinal absorption of sugars and amino acids, reduced immune response, and increased protein catabolism (Santidrian, 1981;Santidrian and Marzo, 1989;Marzo et al, 2002). However, with better understanding of the chemical composition and biological activity of tannins (Mueller-Harvey, 2006), tannin is now known to play a beneficial antioxidant role, preventing lipid peroxidation (Laughton et al, 1991;Morel et al, 1993;Caraceni et al, 1997;Lopes et al, 1999;Rajalakshmi et al, 2001;Glahn et al, 2002) reported that at 0.5% inclusion rate, chestnut tannins had positive effects on carcass characteristics, meat quality, lipid oxidation and fatty acid composition in rabbits.…”

Section: Introductionmentioning

confidence: 99%

Effects of Tannic Acid on Performance and Fatty Acid Composition of Breast Muscle in Broiler Chickens Under Heat Stress

Ebrahim

Liang

Jahromi

et al. 2015

Italian Journal of Animal Science

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One hundred twenty day-old broiler chicks (Cobb 500) were randomly assigned into 4 treatment groups to investigate the effects of tannic acid supplementation (TA) on fatty acid composition in breast muscle of broilers under chronic heat exposure conditions. Five pen replicates of 6 chicks each were assigned to each of the following 4 dietary treatments: i) basal diet containing no TA at 25°C (CL); ii) basal diet containing no TA at 35°C (CH); iii) basal diet supplemented with 1% TA at 25°C (TL); and iv) basal diet supplemented with 1% TA at 35°C (TH). At the end of the 5-week experiment, breast muscle samples were collected to examine the fatty acid composition. Results showed that temperature, TA and their interaction effect significantly decreased body weight gain and feed intake. In addition, feed conversion ratio (FCR) significantly increased under high temperature, and addition of TA under high temperature did not improve the FCR. The effects of temperature, TA and their interaction on the saturated and unsaturated fatty acids were not significant (P>0.05). However, monounsaturated fatty acids significantly reduced by adding TA to the diet. Generally, TA improved the fatty acid profile of breast muscle of broilers under heat stress in comparison to the heat stressed chickens, which did not receive TA. Hence, it seems that dietary TA supplementation can be applied as a biological antioxidant for poultry nutrition in hot climatic conditions.

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“…For instance, calcium stimulates generation of ROS at specific sites of the inner mitochondrial membrane, where they attack protein thiols, thereby opening permeability transition pores (Fagian et al 1990; Kowaltowski et al 1996Kowaltowski et al , 1998. One crucial effect of ROS is known to be the oxidative damage of nucleic acids (Cross et al 1987;Lemasters et al 1992), substantiated by single-strand breaks and inter/intrastrand crosslinks (Caraceni et al 1997). The persistence of ROS-mediated DNA alterations might lead to serious and long-lasting consequences, as suggested by the association between the persistence of ROS-mediated DNA alterations and mutagenic events (Emerit 1994).…”

mentioning

confidence: 99%

DNA damage associated with ultrastructural alterations in rat myocardium after loud noise exposure.

Lenzi

Frenzilli

Gesi

et al. 2003

Environ Health Perspect

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Noise exposure causes changes at different levels in human organs, particularly the cardiovascular system, where it is responsible for increasing heart rate, peripheral vascular resistance, and blood pressure. In this study, we evaluated the effect of noise exposure on DNA integrity and ultrastructure of rat cardiomyocytes. The exposure to loud noise (100 dBA) for 12 hr caused a significant increase of DNA damage, accompanied by swelling of mitochondrial membranes, dilution of the matrix, and cristolysis. These alterations were concomitant with increased in situ noradrenaline levels and utilization. Genetic and ultrastructural alterations did not decrease 24 hr after the cessation of the stimulus. An elevated oxyradical generation, possibly related to altered sympathetic innervation, is hypothesized as responsible for the induction and persistence of noise-induced cellular damage.

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Proteins but not Nucleic Acids are Molecular Targets for the Free Radical Attack During Reoxygenation of Rat Hepatocytes

Cited by 39 publications

References 20 publications

Eicosapentaenoic acid protects against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced hepatic toxicity in cultured rat hepatocytes

Eicosapentaenoic acid protects against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced hepatic toxicity in cultured rat hepatocytes

Effects of Tannic Acid on Performance and Fatty Acid Composition of Breast Muscle in Broiler Chickens Under Heat Stress

DNA damage associated with ultrastructural alterations in rat myocardium after loud noise exposure.

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