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Effect of Boron on the Potassium Dichromate Induced Oxidative Damage in Brain Tissue of Sprague Dawley Rats




Effect of Boron on the Potassium Dichromate Induced Oxidative Damage in Brain Tissue of Sprague Dawley Rats

Zeynep Soyer Sarıca1*, Meryem Eren2 and Meryem Senturk2

1Experimental Research Center Melikgazi, University of Erciyes, 38039 Kayseri,Turkey

2 Department of Biochemistry, Faculty of Veterinary Medicine, University of Erciyes, Melikgazi, 38039 Kayseri, Turkey


In this study the effect of the trace mineral, boron (B) was determined on the potassium dichromate induced oxidative damage in the brain tissue of Sprague Dawley rats. Malondialdehyde (MDA) levels and activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) enzymes were estimated in the brain tissues of the Sprague Dawley rats. Compared to the control groups, a significant increase in the brain tissue MDA level of the group which received only 10 mg/kg K2Cr2O7 was observed, whereas no statistically significant change was detected in SOD, CAT and GSH-Px enzyme activities. It was further observed that after administration of Boron at 5 and 10 mg/kg the lipid peroxidation in brain tissue of K2Cr2O7-treated rats decreased significantly, but no significant changes were observed in the levels of antioxidant enzyme. It can be concluded that administration of 5 and 10 mg/kg B may have beneficial effects against lipid peroxidation caused by K2Cr2O7 in the brain tissue of rats.

Article Information

Received 27 December 2017

Revised 03 March 2018

Accepted 28 April 2018

Available online 12 July 2019

Authors’ Contribution

ZSS planned, conducted and reviewed the study. ME planned the study, reviewed and interpreted results. MŞ planned, conducted and reviewed the manuscript.

Key words

Brain, Boron, Oxidative stress, Potassium dichromate, Rat


* Corresponding author:

0030-9923/2019/0005-1905 $ 9.00/0

Copyright 2019 Zoological Society of Pakistan


Two important forms of chromium, Cr(III) and Cr(VI) are biologically quite active chromium ions and Cr(VI) has a high toxicity for oxidative stress. Chromium (VI) which passes fast through anionic channels to spread in the cell is produced with industrial processes. In case of exposure, it reacts with the oxygen in the body causing serious damages such as allergic dermatitis, acute and chronic toxicity, neurotoxicity, dermatoxicity, genotoxicity, carcinogenicity and immunotoxicity (Akinwumi et al., 2016; Deraz et al., 2016; Dashti et al., 2016). Chromate ions [(CrO4)-2] are neutral aqueous solutions of Cr(VI) and aggressive compound that can pass cell membrane through nonionic anionic channels (Bagchi et al., 1997). There are many studies that explain the effects of chromium forms on tissue damage (Stohs and Bagchi, 1995; Soudani et al., 2012; Bashandy et al., 2016; Wang et al., 2016). Zhang and Li (1987) reported in their epidemiological study conducted in Liaoning region of China that total cancer cases, stomach cancer and lung cancer cases increased as a result of contamination of water sources by a Cr mine in the region. Linos et al. (2011) reported that there was increase in liver, lung and kidney cancers as a result of contamination of water sources with Cr (VI) for at least 20 years in the Oinofita region of Greece. Especially Cr (VI) compounds such as potassium dichromate (K2Cr2O7), sodium chromate and chromic acid are widely used in the leather industry, electro-coating industry, welding workshops, chrome coating industry and paint and coating industry. Chromium effects can be seen in the tests conducted with the blood, urine and some tissues of the people working in these industries. Lung and sinus cancer can develop when the person is exposed through inhalation and accidental or intentional high dose Cr exposure can cause potentially fatal respiratory, cardiovascular, gastrointestinal, hepatic, renal and neurological consequences. Additionally, it can have negative effects on reproduction and fetal development (Garcia-Nino et al., 2015).

Boron (B) is an essential element for humans and animals and it is considered to play an active role in various metabolisms in the body, have important functions in the brain together with the endocrine system, have effects of physical performance and have potential effect on bone tissue diseases such as osteoporosis, osteoarthritis (Nielsen, 1997). The daily B requirement of humans can be 0.5 mg/day (Nielsen et al.,1988). Boron is taken into the body with food and drinks, and through inhalation and skin (Becking et al., 1998). However, it is used for therapeutic purposes for skin diseases such as eczema and psoriasis (Demirtaş, 2010).

Penland (1994) concluded that daily intake of 3.25 mg B in post menopausal women led to an improvement in motor activities, reaction times, short and long term memory and memory skills. When taken in lower doses people were found to show lower levels of psychomotor and cognitive performance. Recent studies found that B has an important role in many mechanisms such as mineral metabolism, regulation of endocrine functions, vitamin D metabolism, bone metabolism and lipid metabolism in humans and animals and a positive effect on carbohydrate and protein structures (Hegsted et al.,1991; Rainey, 1999; Eren, 2004; Eren et al., 2006; 2012; Kurtoğlu et al., 2005; Çiftçi et al., 2013; Yıldız et al., 2013; Nielsen, 2014).

This study aims to determine the effect of the trace mineral B, on the oxidative stress caused by K2Cr2O7 in Sprague Dawley rats.



Animal material

The ethics approval for the study was obtained from the Animal Experiment Ethics Committee of Erciyes University in Turkey (ERÜ HADYEK) (decision no: 12/56 dated 11.04.2012). In this study, 60 Sprague-Dawley female rats (average weight 250-300g) obtained from the Experimental Research Center of Erciyes University Turkey were used. Rats were kept in the accommodation conditions for experimental animals at a controlled temperature (21±2 ˚C), humidity (50 ±5%), lighting (12 hours of light, 12 hours of darkness) and ad libitum feeding.

Study groups

Sixty female Sprague Dawley rats weighing 200-250 g, were divided into six groups of 10 in each group. The rats in the first group were given 2 ml distilled water and this group was assigned as the control group; 2nd group received 5 mg/kg (live weight)/day B; 3rd group received 10 mg/kg (live weight)/day B; 4th group received 10 mg/kg K2Cr2O7; 5th group received 10 mg/kg K2Cr2O7 + 5 mg/kg (live weight)/day B; 6th group K2Cr2O7 + 10 mg/kg (live weight)/day B. Distilled water, K2Cr2O7 and B (in boric acid form) were given to the animals via gavage for two weeks. K2Cr2O7 dose used in the study was based on the results of the study of Mohammed and Saber (2011) while B doses used in this study were based on the results of the study of Price et al. (1997). Investigators determined that B supplement up to 10 mg/kg (live weight) would not have any adverse effect. Negative effects could be seen in doses exceeding 10 mg. No observed adverse effect level (NOAEL) was 10 mg B/kg live weight/day and the lowest observed adverse effect level (LOAEL) was 13 mg B/kg live weight/day at which toxicity signs might develop based on blood B levels.

Analysis methods

At the end of the experiment, animals were sacrificed under ketamine/xylazine anesthesia and their brain tissues were removed, washed with cold distilled water, homogenized in phosphate buffer pH 7.4 (Heidolph, Silent Crusher M), centrifuged at 15,000 rpm, at +4°C for 45 min and supernatant was transferred to eppendorf tubes. All samples were stored at -80°C until analysis.

Malondialdehyde levels and superoxide dismutase (SOD), catalase (CAT) and glutation peroxidase (GSH-Px) enzyme activities were measured in the brain tissue samples. Tissue MDA analyses were done with the method developed by Yoshioka et al. (1979) CAT analyses with the spectrophotometric method developed by Luck (1965), SOD activity analyses were done with the method reported by Sun et al. (1988), GSH-Px activity measurements were done with the spectrophotometric method developed by Paglie and Valentine (1967).

Statistical analyses of data were done with the SPSS 20.0 program for Microsoft. Differences between groups were determined with one way variance analysis (ANOVA). When F value was significant, Duncan’s Multiple Range Test was conducted to identify the group the difference came from. Data are provided as the mean and standard error of mean.



Compared to the control groups, a significant increase (P<0.001) in the brain tissue MDA level of the group which received only K2Cr2O7 was observed. These MDA levels which increased in the brain tissues of rats administered K2Cr2O7 decreased significantly (P<0.001) with 5 and 10 mg/kg B administration. On the other hand the brain tissue SOD, CAT and GSH-Px enzyme activities of the group of rats that were administered only K2Cr2O7 decreased though not statistically significant compared to the control groups. However, administration of 5 and 10 mg/kg B to the K2Cr2O7 groups, although not statistically significant, increased these antioxidant enzyme activities to a level close to the values of the control group (P>0.05; Table I).



In recent years, studies which use herbal (Mohammed and Saber, 2011; Soyer-Sarıca and Liman, 2016),

Table I.- Effect of boron on K2Cr2O7 induced oxidative stress parameters in brain tissue of Sprague Dawley rats.

Oxidative stress parameters





K2Cr2O7 +

5 mg/kg B

K2Cr2O7 +

10 mg/kg B



5 mg/kg

10 mg/kg

MDA(nmol /mg-protein)


13.09± 1.85b

13.48± 1.64b

17.07± 1.42b

24.74 ±1.88a




0.000 ***



4.97± 0.88

3.91± 0.52

4.04± 0.36

3.83± 0.33







5.46± 0.61

5.58± 1.04

5.04± 0.76

3.18± 0.63







26.59± 10.64

36.05± 4.92

35.78 ±4.02

23.27± 3.13





a,b, Values within each row with different superscripts differ significantly; ***, P<0.001


MDA, Malondialdeyde; SOD, Superoxide dismutase; CAT, Catalase; GSH-Px, Glutathione peroxidase.

xenobiotic (Kanbur et al., 2016) and mineral substances (Çolak et al., 2011; Eren and Şentürk, 2016) have been common as protective agents against environmental toxicity. Hexavalent Cr compounds are highly toxic and can penetrate into cells and cause cancerogenous, cytotoxicity, DNA destruction and lipid peroxidation (Rasool et al., 2014). Limited number of studies about the potential harmful effects of Cr(VI) on brain tissue was found (Travacio et al., 2001; Garcia-Nino et al., 2015; Dashti et al., 2016; Salama et al., 2016; Hao et al., 2017).

In the cerebellar granule neuron cell culture study (Dashti et al., 2016), mature and immature cerebellar cells were exposed to Cr and the investigators reported that mature cells were more affected by Cr exposure and their lipid peroxidation and GSH-Px activities increased.

Hao et al. (2016) orally administered K2Cr2O7 (6% LD50) for 42 days and reported that it caused a histologically degenerative effect in brain cell structures. Additionally compared to the control group, there was a statistically significant increase in the MDA levels of the group that was administered K2Cr2O7. These investigators concluded that long term exposure to Cr (VI) can cause histological changes and oxidative stress in the chicken brain and this can occur with the accumulation of Cr (VI) in the brain tissue. It is claimed that Hexavalent Cr compounds increase the production of nitric oxide and reactive oxygen species (ROS) which lead to an increase in MDA levels (Bagchi et al., 2001; Hao et al., 2016; Stohs and Bagchi, 1995).

Travacio et al. (2001) found a significant increase in brain tissue MDA levels when they gave 25 mg/kg K2Cr2O7 with drinking water for 3 days. Rasool et al. (2014) found an increase in serum MDA levels, and a decrease in SOD, CAT and GSH-Px activities when male rats were orally administered 5 mg/kg K2Cr2O7 for 30 and 60 days. Histopathologically, these investigators demonstrated that K2Cr2O7 increased reactive oxygen species in rats’ testicles causing a significant increase in lipid peroxidation.

Salama et al. (2016) intranasally administered three different doses of K2Cr2O7 (0.5, 1 and 2 mg/kg, live weight) and reported that the highest brain MDA level was in 2 mg/kg group and no change was observed in other doses. In another study conducted in rats i.p administration of a single 15 mg/kg dose of K2Cr2O7 triggered oxidative stress in liver (MDA, GSH, SOD, CAT levels) but did not cause oxidative stress and histopathological change in organs such as brain, heart, lung, kidney, spleen. In this study it was claimed that the fact that K2Cr2O7 did not show any toxic effect in the above mentioned tissues could be associated with the administration method of the element, absorption through portal circulation, low dose or single dose administration, and how long it was administered (Garcia-Nino et al., 2015).

Boron trace element is considered to reduce oxidative stress when nicotinamide adenine dinucleotide phosphate (NADP) increases reduced glutathione (GSH) amount in cells (Uçkun, 2013). Hoang et al. (2017) reported that they provided protection from oxidative stress using a synthetic boric acid derivative mask they developed, by restricting angiogenesis stimulation which is effective in amyotrophic lateral sclerosis (ALS), a neurodegenerative disease.

Şahin et al. (2012) gave rats a normal diet, a high fat diet and a diet supplemented with B for 12 weeks and recorded that rats that consumed high fat diet had elevated levels of brain tissue MDA; and that these values in rats fed with the diet supplemented with B decreased similar to the control group. Çolak et al. (2011) administered 3.25, 36 and 58.5 mg/kg boric acid (4.375, 6.3 and 10.23 mg/kg, B) against the damage that aluminium chloride could cause in the brain. They reported that the lowest dose of boric acid had a protective effect on neurons in the brain tissue and in other doses it caused damage in the brain tissue. In another study, rats were administered different doses of B (5, 10 and 20 mg/kg/day) i.p against lipid peroxidation caused by cyclophosphamide and administration of B had a positive effect on the increased MDA values and reduced antioxidant enzymes in the brain tissue after the cyclophosphamide administration (İnce et al., 2014). Çoban et al. (2015) demonstrated that oxidative stress in the tissues caused by 100 mg/kg/day malathion in rats could be prevented with different doses of B (5, 10 and 20 mg/kg/day).

Küçükkurt et al. (2015) administered 100 mg/kg B against adverse effects of arsenic given to male and female Wistar albino rats in drinking water for 28 days and reported a significant decrease in brain tissue MDA levels of the rats which were exposed to arsenic and B. These investigators determined that a decrease occurred in brain tissue SOD and CAT enzyme activities in male rats with arsenic administration and that administration of B did not have any effect on this decrease. Furthermore, they found that neither arsenic group not arsenic plus B group did not cause any change in these antioxidant enzymes in female rats. In another study, male Wistar albino rats which had diabetes induced with streptozotocin (STZ), 5 and 10 mg/kg (live weight) B (in boric acid form) significantly reduced serum MDA levels that were increased with diabetes but its effect on total antioxidant capacity was not statistically significant and just brought the total antioxidant capacity levels close to the the values in the control group and this could be due to the B’s reducing effect on lipid peroxidation (Çakır et al., 2018). In this study, it was observed that brain tissue SOD, CAT and GSH-Px activities were not affected.



In conclusion, comparable to the findings of some studies (Travacio et al., 2001; Dashti et al., 2016; Salama et al., 2016; Hao et al., 2016), 10 mg/kg K2Cr2O7 orally administered for two weeks in rats increased the production of reactive oxygen types and thus increased brain tissue MDA levels. On the other hand, increased brain tissue MDA levels caused by K2Cr2O7 decreased after administering 5 and 10 mg/kg B due to the protective effect of this element against lipid peroxidation (İnce et al., 2014; Çoban et al., 2015; Küçükkurt et al., 2015; Çakır et al., 2018). The reason why K2Cr2O7 did not have an adverse effect on antioxidant enzymes in the brain tissue, as also reported by Garcia-Nino et al. (2015) could be the administration method of this agent, its absorption through portal circulation, applied doses and for how long it was given. In conclusion B can have a protective effect against various agents that could cause oxidative stress.



This material of study was provided by Erciyes University Research Fund Project no: TSA-12-4017.


Statement of conflict of interest

Authors have declares that there is no conflict.



Akinwumi, K.A., Osifeso, O.O., Jubril, A.J., Adedoja, A.W., Ogunbiyi, E.T., Adebo, F.M., Adesina, I.O. and Odunola, O.A., 2016. Potassium dichromate toxicities: Protective effect of methanol extract of Corchorus olitorius in albino rats. J. med. Fd., 19:457-65.

Bagchi, D., Vuchetich, P.J., Bagchi, M., Hassoun, E.A., Tran, M.X., Tang, L. and Stohs, S.J., 1997. Induction of oxidative stress by chronic administration of sodium dichromate [chromium VI] and cadmium chloride [cadmium II] to rats. Free Radic. Biol. Med., 22:471-8.

Bagchi, D., Bagchi, M. and Stohs, S.J., 2001. Chromium (VI)-induced oxidative stress, apoptotic cell death and modulation of p53 tumor suppressor gene. Mol. Cell Biochem., 222:149-58.

Bashandy, S.A.E., Amin, M.M., Morsy, F.A. and El-Marasy S.A., 2016. Amelioration of the nephrotoxic effect of potassium dichromate by whey protein and/or Nigella sativa oil in male albino rats. J. appl. Pharm. Sci., 6: 44-50.

Becking, G.C. and Chen, B.H., 1998. International Programme on Chemical Safety (IPCS) environmental health criteria on boron human health risk assessment. Biol. Trace Elem. Res., 66:439-52.

Bilgiç, M. and Dayık, M., 2013. Boron properties and advantages of use in the textile industry. Electr. J. Textile Technol., 7:27-37.

Çakır, S., Eren, M., Şentürk, M. and Soyer-Sarıca, Z., 2018. The effect of boron on some biochemical parameters in experimental diabetic rats. Biol. Trace Elem. Res., 184: 165-172.

Çiftçi, H.B. and Yıldırım, İ., 2013. Effect of estradiol-17β on serum mineral concentrations of female japanase quail. J. Toxicol. Sci., 37: 1-7.

Çoban, F.K., İnce, S., Küçükkurt, İ., Demirel, H.H. and Hazman, O., 2015. Boron attenuates malathion-induced oxidative stress and acetylcholinesterase inhibition in rats. Drug. Chem. Toxicol., 38:391-299.

Çolak, S., Geyikoglu, F., Keles, O.N., Türkez, H., Topal, A. and Unal, B., 2011. The neuroprotective role of boric acid on aluminum chloride-induced neurotoxicity. Toxicol. Ind. Hlth., 27:700-710.

Dashti, A., Soodi, M. and Amani, N., 2016. Cr (VI) induced oxidative stress and toxicity in cultured cerebellar granule neurons at different stages of development and protective effect of Rosmarinic acid. Environ. Toxicol., 31:269-277.

Demirtaş, A., 2010. Importance of boron for human health and nutrition. J. Agric. Fac. Atatürk Univ., 41:75-80.

Deraz, E.M., Abd-Elhamid, A.M.E. and Fahmi, A.N., 2016. Histological and ultrastructural study of the effect of potassium dichromate with evaluation of potential protective role of vitamin C on submandibular salivary gland of rats. J. Am. Sci., 12:84-90.

Eren, M., 2004. Effects of Boron biological importance and metabolism. J. Fac. Vet. Med. Univ. Erciyes, 1: 55-59.

Eren, M., Kocaoğlu-Güçlü, B., Uyanık, F. and Karabulut, N., 2006. The effects of dietary boron supplementation on performance, carcass composition and serum lipids in Japanese quails. J. Anim. Vet. Adv., 5: 1105-1108.

Eren, M., Uyanık, F., Kocaoğlu-Güçlü, B. and Çınar, M., 2012. Effects of dietary boric acid and borax supplementation on growth performance and some biochemical parameters in broilers. Rév. Méd. Vét., 163:546-551.

Eren, M. and Şentürk, M., 2016. The effects of potassium dichromate and boron on oxidative stress and DNA damage in rats. 8. National Veterinary Congress of Biochemistry and Clinical Biochemistry. Uludağ Üniversitesi, Bursa, Türkiye. pp. 120-121.

García-Niño, W.R., Zatarain-Barrón, Z.L., Hernández-Pando, R., Vega-García, C.C., Tapia, E. and Pedraza-Chaverri, J., 2015. Oxidative stress markers and histological analysis in diverse organs from rats treated with a hepatotoxic dose of Cr (VI): Effect of curcumin. Biol. Trace Elem. Res., 167:130-145.

Hao, P., Zhu, Y., Wang, S., Wan, H., Chen, P., Wang, Y., Cheng, Z., Liu, Y. and Liu, J., 2017. Selenium administration alleviates toxicity of Chromium (VI) in the chicken brain. Biol. Trace Elem. Res., 178:127-135.

Hegsted, M., Keenan, M.J., Siver, F. and Wozniak, P., 1991. Effect of boron on vitamin D deficient rats. Biol. Trace Elem. Res., 28: 243-255.

Hoang, T.T., Smith, T.P. and Raines, R.T., 2017. A Boronic acid conjugate of angiogenin that shows ROS-responsive neuroprotective activity. Angew. Chem. Int. Ed. Engl., 56:2619-2622.

İnce, S., Küçükkurt, İ., Demirel, H.H., Acaroz, D.A., Akbel, E. and Cigerci, I.H., 2014. Protective effects of boron on cyclophosphamide induced lipid peroxidation and genotoxicity in rats. Chemosphere, 108:197-1204.

Kanbur, M., Siliğ, Y., Eraslan, G., Karabacak, M., Soyer-Sarıca, Z. and Şahin, S., 2016. The toxic effect of cypermethrin, amitraz and combinations of cypermethrin-amitraz in rats. Environ. Sci. Pollut. Res. Int., 23: 5232-5242.

Kurtoğlu, F., Kurtoğlu, V., Çelik, İ., Keçeci, T. and Nizamlıoğlu, M., 2005. Effects of dietary boron supplementation on biochemical parameters, peripheral blood lymphocytes, splenic plasma cells and bone characteristics of broiler chicks given diets with adequate or inadequate cholecalciferol (vitamin D3) content. Br. Poult. Sci., 46: 87-96.

Küçükkurt, İ., İnce, S., Demirel, H.H., Türkmen, R., Akbel, E. and Çelik, Y., 2015. The effects of boron on arsenic-ınduced lipid peroxidation and antioxidant status in male and female rats. J. Biochem. Mol. Toxicol., 29:564-571.

Linos, A., Petralias, A., Christopi, C.A., Christoforidou, E., Kouroutou, P., Stoltidis, M., Veloudaki, A., Tzala, E., Makris, K.C. and Karagas, M.R., 2011. Oral ingestion of hexavalent chromium through drinking water and cancer mortality in an industrial area of Greece-an ecological study. Environ. Hlth., 10:50.

Luck, H.S., 1965. Catalase. In: Methods in analysis (ed. H.U. Bergmeyer), pp. 388. New York, USA.

Mohammed, N.E. and Saber, R.A., 2011. Effect of aqueous extract of Damsissa (Ambrosia maritima) on the biochemicl chamges induced by potassium dichromate in rats. J. Am. Sci., 7:234-242.

Nielsen, F.H., Shuler, T.R., Zimmerman, T.J. and Uthus, E.O., 1988. Dietary magnesium, manganase and born affect the response of rats to high dietary aluminium. Magnesium, 7: 133-147.

Nielsen, F.H., 1997. Boron in human and animal nutrition. Pl. Soil, 193: 199-208.

Nielsen, F.H., 2014. Update on human health effects of boron. J. Trace Elem. Med. Biol., 28: 383-387.

Paglie, D. and Valentie, W.N., 1967. Studies on the quanlitative and quantitative characterization of erytrocyte glutathione peroxidase. J. Lab. Med., 70: 158-169.

Penland, J.G., 1994. Dietary boron, brain function, and cognitive performance. Environ. Hlth. Respect., 1029: 65-67.

Price, C.J., Strong, P.L., Murray, F.J. and Goldberg, M.M., 1997. Blood boron concentrations in pregnant rats fed boric acid throughout gestation. Reprod. Toxicol., 11: 6: 833-842

Rainey, C.J., Nyquist, L.A., Christensen, R.E., Strong, P.L., Culver, B.D. and Coughlin, J.R., 1999. Daily boron intake from the American diet. J. Am. Diet Assoc., 99: 335-340.

Rasool, M., Zaigham, K. and Malik, A., 2014. Potential reproductive health effects and oxidative stress associated with exposure to potassium dichromate (K2Cr2O7) and magnesium sulphate (MgSO4) in male mice. Pak. J. Med, Sci., 30: 819-823.

Salama, A., Hegazy, R. and Hassan, A., 2016. Intranasal chromium ınduces acute brain and lung ınjuries in rats: Assessment of different potential hazardous effects of environmental and occupational exposure to chromium and ıntroduction of a novel pharmacological and toxicological animal model. PLoS One, 11: 1-20.

Soudani, N., Troudi, A. and Amara, I.B., 2012. Ameliorating effect of selenium on chromium (VI)-induced oxidative damage in the brain of adult rats. J. Physiol. Biochem., 68:397-409.

Soyer-Sarıca, Z. and Liman, B.C., 2016. The effects of pomegranate seed oil on pentachlorophenol toxicity in lipid peroxidation and biochemical parameters in rats. J. Fac. Vet. Med. Univ. Erciyes, 13:109-119.

Stohs, S.J. and Bagchi, D., 1995. Oxidative mechanisms in the toxicity of metal ions. Free Radic. Biol. Med., 18:321-336.

Sun, Y., Oberley, L.W. and Li, Y.A.A., 1988. Simple for clinical assay of superoxide dismutase. Clin. Chem., 34: 497-500.

Şahin, N., Akdemir, F. and Orhan, C., 2012. A novel nutritional supplement containing chromium picolinate, phosphatidylserine, docosahexaenoic acid, and boron activates the antioxidant pathway Nrf2/HO-1 and protects the brain against oxidative stress in high-fat-fed rats. Nutr. Neurosci., 15: 42-47.

Travacio, M., Polo, J.M. and Llesuy, S., 2001. Chromium (VI) induces oxidative stress in the mouse brain. Toxicology, 11:139-148.

Uçkun, Z., 2013. An essantial component: Daily intake of Boron and physiological effects. J. Turk. Sci., 6: 119-123.

Wang, Y., Wu, W. and Yao, C., 2016. Elevated tissue Cr levels, increased plasma oxidative markers, and global hypomethylation of blood DNA in male Sprague-Dawley rats exposed to potassium dichromate in drinking water. Environ. Toxicol., 31: 1080-1090.

Woods, W.G., 1994. An introduction to boron: history, sources, uses, and chemistry. Environ. Hlth. Perspect., 102: 5–11

Yıldız, G., Köksal, B.H. and Sızmaz, O., 2013. Effects of dietary boric acid addition on growth performance, cholesteromania, some carcass and tibia characteristics in different rearing periods in broiler chickens. Rev. Med. Vet., 164: 219- 224.

Yoshioka, T., Kawada, K. and Schimada, T., 1979. Lipid peroxidation in material and cord blood and protective mechanism aganist activated-oxigen toxicity in the blood. Am. J. Obstet. Gynecol., 135: 372-376.

Zhang, J. and Li, X., 1987. Chromium pollution of soil and water in Jinzhou. Chinese J. Prevent. Med., 21:262-264.

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