Protective effects of zinc salts on TPA-induced hepatic and brain lipid peroxidation, glutathione depletion, DNA damage and peritoneal macrophage activation in mice

Bagchi, Debasis; Vuchetich, Philip J.; Bagchi, Manashi; Tran, Minh X.; Krohn, R. L.; Ray, Sidhartha D.; Stohs, Sidney J.

doi:10.1016/s0306-3623(97)00072-4

Cited by 51 publications

(30 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Bioavailability of zinc methionine chelate is higher by 206% compared to supplementation with zinc sulphate (Wedekind et al 1992). Zinc administered in this form offers higher protection against free radicals compared to zinc salts (Bagchi et al 1998).…”

Section: Discussionmentioning

confidence: 99%

Effect of inorganic and organic zinc supplementation on coccidial infections in goat kids

et al. 2011

View full text Add to dashboard Cite

The aim of this study was to identify the effect of zinc-enriched diet fed to goats and their kids on the number of Coccidia oocysts shed by kids, on clinical signs of coccidiosis, weight gains, and kids' blood plasma concentration of zinc. A total of 22 goat kids were divided into 4 groups of 5 or 6 animals. Goats and kids from the control group did not receive any additional zinc, the second group was supplemented with inorganic zinc (zinc oxide), the third group was given zinc lactate, and the fourth group received chelated zinc. Samples of kids' faeces were taken weekly from 3 to 9 weeks of their age (a total of 7 samples were taken). Samples of faeces were examined by a quantitative method to detect the number of oocysts. Kids were weighed weekly and their blood was taken in order to determine zinc concentrations in blood plasma. Animals from the group supplemented with zinc chelate and zinc lactate shed a significantly (p ≤ 0.05) lower number of oocysts (13.4% and 11.9%, respectively) compared to the number of oocyst shed by control and zinc oxide supplemented groups (25% and 49.7%, respectively). Shedding of oocysts was not accompanied by clinical symptoms of coccidiosis in any of the groups. Kids supplemented with zinc chelate showed significantly highest weight gains and blood plasma concentration of zinc (p ≤ 0.05) as compared to control and inorganic zinc supplemented groups. Organic zinc is to be recommended to be used as a prophylaxis against coccidiosis in goat kids. Eimeria, coccidiosis, weight gain, zinc chelate, zinc lactate, zinc oxideInfections caused by Eimeria coccidia belong to the most significant protozoal infections. In goat kids, six specific Eimeria species were detected, namely E. arloingi, E. ninakohlyakimovae, E. christenseni, E. hirci, E. caprina and E. alievi. Their prevalence is considered to be global. In Spain, coccidiosis affects 96.1% goat kids fed milk (Ruiz et al. 2006). In northern Jordan, coccidiosis occurs in 85% local goats and 54% of them show concurrent infection with multiple Eimeria species. Incidence of concurrent infection was significantly higher in kids (66%) than in animals over 1 year of age (49%) (Mahmoud and Hossan 2003). Prevalence of coccidia in the U.S.A. was 100% (n = 318); in Australia, coccidia were detected in 97% kids out of 497 (Reeg et al. 2005). In the Czech Republic, Strnadová et al. (2008) found coccidia in 54% kids less than 4 months old.The course of clinical coccidiosis in goat kids can be acute, subacute, chronic or latent. The first symptoms of acute coccidiosis include raised temperature, watery diarrhea containing blood and particles of intestinal mucosa, mucosal anaemia, conjunctivitis and rhinitis. Mahmoud and Hossan (2003) reported up to 58% mortality of kids. Animals from 1 to 3 months of age are most susceptible and they shed oocysts most intensively between 5 and 8 weeks of age (Reeg et al. 2005). The course of infection is affected by the number of oocysts being shed. Coccidiosis is considered to be clinical when more tha...

show abstract

Section: Discussionmentioning

confidence: 99%

Effect of inorganic and organic zinc supplementation on coccidial infections in goat kids

et al. 2011

View full text Add to dashboard Cite

show abstract

“…Zinc deficiency could cause oxidative damage to lipids, proteins, and DNA (Bagchi et al, 1998;Burke and Fenton, 1985;Virgili et al, 1999). In vitro studies have shown that depletion of intracellular Zn 2+ by treatment of cells with TPENinduced apoptosis (Adler et al, 1999;Ahn et al, 1998;Martin et al, 1991;Tjen et al, 2002;Treves et al, 1994;Yui et al, 2002;Zalewski et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Cytotoxic effects of intra and extracellular zinc chelation on human breast cancer cells

Hashemi

Ghavami

Eshraghi

et al. 2007

European Journal of Pharmacology

124

View full text Add to dashboard Cite

Zinc is an essential trace element with cofactor functions in a large number of proteins of intermediary metabolism, hormone secretion pathways, immune defence mechanisms, and as a cofactor of transcription factors it is also involved in the control of gene expression. Our study demonstrates that the modulation of intra and extracellular zinc alone is sufficient to induce metabolic changes or even apoptosis in two model human breast cancer cell lines MCF-7 and MDA-MB468. Treatment of breast cancer cells with different concentrations of a cell membrane permeable zinc chelator, N,N,N′,N′-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) and the membrane impermeable zinc chelator, diethylenetriaminepentacetic acid, (DTPA) resulted in a significant increase of cell death. Features of apoptosis, such as chromatin condensation and nuclear fragmentation accompanied the DTPA and TPEN-induced cell death. A significant increase in the activity of caspase-9 was observed in both cell lines; whereas, caspase-3 activity was only increased in MDA-MB468 cells since caspase-3 is not expressed in MCF-7 cells. Caspase-8 activation was negligible in both cell lines. Addition of Zn 2+ or Cu 2+ prevented DTPA and TPEN-induced cytotoxicity, indicating that both bivalent cations can be replaced functionally to a certain extent in our experimental system. Interestingly, addition of Ca 2+ , or Mg 2+ had no effect. The antioxidant N-Acetyl-L-Cysteine inhibited the cytotoxic effect of DTPA and TPEN, indicating that oxidative stress is the likely mediator of Zn-deficiency-related cell death.

show abstract

“…Consistent with an essential role for zinc in oxidative defense, conditions of zinc deficiency have been associated with evidence of oxidative damage to lipids, proteins and DNA [5][6][7][8][9][10][11]. Zinc deficiency has also been shown to result in marked changes in several arms of the oxidant defense system [5,7,[10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Zinc Status of Human IMR-32 Neuroblastoma Cells Influences Their Susceptibility to Iron-Induced Oxidative Stress

2002

View full text Add to dashboard Cite

The current work tested the hypothesis that the zinc status of a cell influences its sensitivity to iron-induced oxidative stress. Human IMR-32 neuroblastoma cells were cultured for 24 h in nonchelated control media (5 µM zinc; 4.5 µM iron), or in media that was treated with DTPA to reduce its zinc content (chelated media). Chelated media was supplemented with zinc to achieve concentrations of 1.5–50 µM Zn. The media was then replaced with serum-free complex media (0.9 µM Zn) with either no added iron (0.6 µM Fe), or iron (FeCl₃) added at concentrations ranging from 15 to 100 µM. Cells were cultured for an additional 3- to 24-hour period. Over the 24-hour period, cells cultured in the control iron media had good viability, and they displayed the gross morphology typical of these cells in culture. With 100 µM iron, cell viability was low in all groups. After 24 h and at iron concentrations between 15–50 µM, cells that had been cultured in the low zinc-chelated media (1.5 µM Zn) showed a concentration-dependent increase in 5 (or 6)-carboxy-2’7’-dichlorodihydrofluorescein diacetate (DCDCDHF) fluorescence (oxidative stress) and decrease in cell viability. A positive correlation between both parameters was observed (r = 0.92). These cells had altered morphology and high level of nucleosomes suggestive of cell death by apoptosis. These results support the concept that the zinc status of IMR-32 neuroblastoma cells modulates their sensitivity to iron overload.

show abstract

Protective effects of zinc salts on TPA-induced hepatic and brain lipid peroxidation, glutathione depletion, DNA damage and peritoneal macrophage activation in mice

Cited by 51 publications

References 27 publications

Effect of inorganic and organic zinc supplementation on coccidial infections in goat kids

Effect of inorganic and organic zinc supplementation on coccidial infections in goat kids

Cytotoxic effects of intra and extracellular zinc chelation on human breast cancer cells

Zinc Status of Human IMR-32 Neuroblastoma Cells Influences Their Susceptibility to Iron-Induced Oxidative Stress

Contact Info

Product

Resources

About