Metals and apoptosis: Recent developments

Rana, S. V. S.

doi:10.1016/j.jtemb.2008.08.002

Cited by 324 publications

(200 citation statements)

References 189 publications

(195 reference statements)

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“…Copper is essential in low concentrations for plant development and metabolism and plays key roles in the control of genes, oxygen transport, and enzyme activities (Rana., 2008). However, when present in excess, it becomes toxic and inhibits growth.…”

Section: Discussionmentioning

confidence: 99%

The influence of duckweed species diversity on ecophysiological tolerance to copper exposure

et al. 2015

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Section: Discussionmentioning

confidence: 99%

The influence of duckweed species diversity on ecophysiological tolerance to copper exposure

et al. 2015

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“…A role of regulative (helper lymphocytes, cytokines) and effector (macrophages) components of immunity is important in the host defence against parasite. These cells are also target structures for heavy metal effects (Shen et al, 2001;Rana 2008). Mice are monogastric animals in which the liver and kidneys serve as detoxicating organs that help to filter toxic waste metabolites from the body.…”

Section: Discussionmentioning

confidence: 99%

Effect of heavy metal intoxication on macrophage metabolic activity of mice infected with Ascaris suum

Jalčová

2014

Helminthologia

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SummaryThe effect of heavy metal intoxication on superoxide anion (O 2 -) production and larval burden during experimental Ascaris suum infection was studied. Mice were chronically intoxicated with lead (Pb), cadmium (Cd) or mercury (Hg) and subsequently infected with A. suum. The metabolic activity of peritoneal macrophages in mice intoxicated with Pb was suppressed and subsequent parasitic infection did not change this inhibition. Cd intoxication increased the superoxide production and also stimulated the activity of this oxygen radical after A. suum infection. Intoxication with Hg had a stimulative effect on the macrophage metabolic activity and subsequent A. suum infection moderately reduced this activity. Parasite burden was different depending on a type of heavy metal intoxication. Pb intoxication moderately increased the parasite burden in the liver and lungs of intoxicated mice. In contrast, Cd and Hg intoxication triggered a marked reduction of A. suum larvae in the liver and lungs of intoxicated mice, respectively. Monitored heavy metals differed in their immunomodulatory effect on metabolic activity of macrophages what also altered the intensity of the parasite infection in the hosts.

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“…Studies in the liver of rats reported increased oxidative stress damage of proteins and protein degeneration caused by Cu (Alexandrova et al, 2008), lipid peroxidation expressed as MDA activity or immunoreactivity (Zhang et al, 2000;Ozcelik and Uzun, 2009) and DNA damage (Gaetke and Chow, 2003;Alexandrova et al, 2007) that finally could lead to apoptotic cell death (Rana, 2008). Lipid peroxidation produced by ROS is considered to be the most likely mechanism to damage proteins, rather than a direct action of ROS generated by Cu or other metals overload (Yamada et al, 1992;Ogihara et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

“…However, the same properties that make Cu essential, when in excess also generate free radicals that can be seriously deleterious to cells (Rana, 2008). Hepatic toxicity, -E-mail: garcia.vaquero@usc.es 1435 caused by Cu overload, is hypothesized to result from redox properties of Cu and is connected with the formation of ROS (Britton, 1996;Luza and Speisky, 1996).…”

Section: Introductionmentioning

confidence: 99%

“…Cu also forms part of the antioxidant defense system of the cells due to its essential role in the Cu-Zn superoxide dismutase (SOD) and caeruloplasmin (Pan and Loo, 2000). Thus, Cu deficiency in cattle is associated with increased oxidative damage (Ward and Spears, 1997;Gengelbach and Spears, 1998;Cerone et al, 2000).However, the same properties that make Cu essential, when in excess also generate free radicals that can be seriously deleterious to cells (Rana, 2008). Hepatic toxicity, -E-mail: garcia.vaquero@usc.es 1435 caused by Cu overload, is hypothesized to result from redox properties of Cu and is connected with the formation of ROS (Britton, 1996;Luza and Speisky, 1996).…”

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Histochemistry evaluation of the oxidative stress and the antioxidant status in Cu-supplemented cattle

García‐Vaquero

Benedito

López‐Alonso

et al. 2012

Animal

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The aim of this paper is to evaluate at a histopathological level the effect of the most commonly used copper (Cu) supplementation (15 mg/kg dry matter (DM)) in the liver of intensively reared beef cattle. This was done by a histochemistry evaluation of (i) the antioxidant capacity in the liver -by the determination of metallothioneins (MT) and superoxide dismutase (SOD) expression -as well as (ii) the possible induction of oxidative damage -by the determination of inducible nitric oxide synthase (iNOS), nitrotyrosine (NITT), malondialdehyde (MDA) and 8-oxoguanine (8-oxo) -that (iii) could increase apoptotic cell death -determined by cytochrome-c (cyto-c), caspase 1 (casp1) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). Liver samples from Cu-supplemented (15 mg Cu sulphate/kg DM, n 5 5) and non-supplemented calves (n 5 5) that form part of other experiments to evaluate Cu status were collected at slaughter and processed for immunohistochemistry and TUNEL. MT expression was diffuse and SOD showed slight changes although without statistical significance. iNOS and NITT positive (1) cells significantly increased, mainly around the central veins in the animals from the Cu-supplemented group, whereas no differences were appreciated for the rest of the oxidative stress and apoptosis markers. Under the conditions of this study, which are the conditions of the cattle raised in intensive systems in NW Spain and also many European countries, routinely Cu supplementation increased the risk of the animals to undergo subclinical Cu toxicity, with no significant changes in the Cu storage capacity and the antioxidant defensive system evaluated by MT and SOD expression, but with a significant and important increase of oxidative damage measured by iNOS and NITT. The results of this study indicated that iNOS and NITT could be used as early markers of initial pathological changes in the liver caused by Cu supplementation in cattle, although more studies in cattle under different levels of Cu supplementation are needed.Keywords: cattle, copper, subclinical toxicity, oxidative stress, antioxidant defense ImplicationsThis study demonstrates an increased oxidative damage (measured by a significant increase of the markers inducible nitric oxide synthase (iNOS) and nitrotyrosine (NITT)) in the liver of intensively reared beef cattle receiving moderate copper (Cu) supplementation. This oxidative damage could be considered as the initial pathological change in the animal before further damage will occur, and thus, the markers iNOS and NITT could be used as early indicators of subclinical Cu toxicity in cattle under these nutritional conditions. IntroductionCopper (Cu) is an essential metal associated with several enzymes (either as a co-factor or as an allosteric component) that acts as an electron transfer intermediate in redox reactions (Uauy et al., 1998) therefore being vital for the normal function of the organisms. Cu in the liver is accumulated bound to metallothioneins (MT), proteins involved in the detox...

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Metals and apoptosis: Recent developments

Cited by 324 publications

References 189 publications

The influence of duckweed species diversity on ecophysiological tolerance to copper exposure

The influence of duckweed species diversity on ecophysiological tolerance to copper exposure

Effect of heavy metal intoxication on macrophage metabolic activity of mice infected with Ascaris suum

Histochemistry evaluation of the oxidative stress and the antioxidant status in Cu-supplemented cattle

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