Toxicology International (Formerly Indian Journal of Toxicology)

Open Access Open Access  Restricted Access Subscription Access
Open Access Open Access Open Access  Restricted Access Restricted Access Subscription Access

Protective Role of S-Adenosyl Methionine (SAMe) in Cadmium Induced Toxicopathological Changes in Wistar Rats


Affiliations
1 Department of Pathology, College of Veterinary Science and Animal Husbandary, Duvasu, Mathura, India
     

   Subscribe/Renew Journal


Cadmium is considered to be one of the most toxic substances in the environment due to its wide range of organ toxicity and long elimination half-life. SAMe is recognized as the major methyl-donor for essential methylation reactions that occur in all living organisms. SAMe has been increasingly utilized as a therapeutic agent in liver and neurological disorders recently. The present study has been devised to explore the alleviating effects of SAMe in cadmium induced toxicopathological changes in rats. The rats were divided into four experimental groups: group I formed the control, group II animals were given cadmium chloride @ 200ppm in distilled water, orally, group III animals were given SAMe @ 1 mg/kg body weight, orally and group IV were given both CdCl2 and SAMe. Six rats from each group were humanely sacrificed at 30th, 60th and 90th day. The quantitative data of body weight, absolute organ weight, cadmium content and oxidative stress parameters was analyzed by Duncan's multiple range tests The group II animals showed most of the pathological changes compared to the rest of the group. The magnitude of lesions in various organs was lesser in group IV where SAMe was given. The severity of lesions increased with the advancement of experiment; most severe pathological changes occurring on the 90th day. The level of cadmium residue in liver and kidneys of rats was also found to be increasing with the time in group II and IV; with group IV showing a relatively lesser increase. Similarly the evaluation of oxidative stress parameters reflected the detrimental effect of cadmium in group II and an alleviating effect of SAMe in group IV. Based on the results obtained, SAMe is found to alleviate the toxicopathological effects of cadmium in rats which needs to be further explored.

Keywords

Cadmium, S-Adenosyl Methionine, Rats, Toxicopathology.
User
Subscription Login to verify subscription
Notifications
Font Size

  • Patrick L. Toxic metals and antioxidants: part II the role of antioxidants in arsenic and cadmium toxicity.(Toxic Metals Part II).Alternative medicine review 2003; 8:106-29.

  • Martelli A, Rousselet E, Dycke C, Bouron A, Moulis, J. M. Cadmium toxicity in animal cells by interference with essential metals.Biochimie 2006; 88: 1807-14.

  • Prodan L. Cadmium Poisoning: II. Experimental Cadmium Poisoning. Journal of Industrial Hygiene 1932; 14: 174-96.

  • Cantoni GL. Biological methylation: selected aspects. Annu. Rev. Biochem. 1975; 44: 435–51

  • Fontecave M, Atta M, Mulliez E. S-adenosylmethionine: nothing goes to waste. Trends in biochemical sciences 2004; 29: 243-9.

  • Gulyasar T, Nurettin A, Cukina S, Sipahi T, Kaymak K, Sener S. Trace elements in a Rat Model of Cadmium Toxicity: the effects of taurine, melatonin and N-Acetyl cysteine. Trakya Univ Tip Derg 2010; 27: 23-7.

  • Lansdown AB. (2013). Cadmium and Mercury. In: The carcinogenicity of metals: human risk through occupational and environmental exposure. Royal Society of Chemistry; 2013. p220.

  • Lee, H. K. (2001). U.S. Patent Application No. 09/927,839.

  • Luna LG. Manual of histologic stainingnmethod of Armed Forces Institute of Pathology. 3rd edn. McGraw Hill Book Company; 1968.

  • Sedlak J, Lindsay RH. Estimation of total protein bound NPSH groups in tissues with Ellaman’s reagent. Anal. Biochem. 1968; 25: 192-205.

  • Bergmeyer HU. Methods for enzymatic analysis 1983; 2:165-6.

  • Rehman, S.U. Lead induced regional lipid peroxidation in brain. Toxico. Lett. 1984; 21: 333-7.

  • Madesh M, Balasubramanian KA. Microtiter plate assay for superoxide dismutase using MTT reduction by superoxide. Indian J. Biochem. Biophys., 1998;35: 184-8.

  • Lowry OH, Rosenbrough NJ, Farr AL, Randall RJ. Protein measurement with the Folin phenol reagent. J. Biol. Chem., 1951; 193: 265-75.

  • Kolmer J, Spaulding EH, Robinson HW. Approved laboratory Techniques. 5th ed., Aplenton Century Gopts. Inc., New York; 1951.

  • Snedecor CW, Cochran WG. Statistical Methods. Iowa State University Press, Ames, Iowa; 1994.

  • Biswas NM, Gupta RS, Chattopadhyay A, Choudhury GR, Sarkar M. Effect of atenolol on cadmium-induced testicular toxicity in male rats. Reproductive Toxicology 2001; 15: 699-704.

  • Koyu A, Gokcimen A, Ozguner F, Bayram DS, Kocak A. Evaluation of the effects of cadmium on rat liver. Molecular and cellular biochemistry 2006; 284: 81-5.

  • Lee YK, Park EY, Kim S, Son JY, Kim TH, Kang WG et al. Evaluation of cadmium-induced nephrotoxicity using urinary metabolomic profiles in Sprague-Dawley male rats. Journal of Toxicology and Environmental Health, Part A, 2014; 77:1384-98.

  • Dzobo K, Naik YS. Effect of Selenium on Cadmium-induced oxidative stress and esterase activity in rat organs. S Afr J Sci, 2013; 109: 1-8.

  • Goering PL, Klaassen CD. Altered subcellular distribution of cadmium following cadmium pretreatment: possible mechanism of tolerance to cadmium-induced lethality. Toxicology and applied pharmacology,1983; 70: 195-203.

  • Yang H, Shu Y. Cadmium transporters in the kidney and cadmium-induced nephrotoxicity. International journal of molecular sciences 2015; 16: 1484-94.

  • Waalkes MP. Cadmium carcinogenesis in review. Journal of inorganic biochemistry. 2000; 79:241-4.

  • Waalkes MP. Cadmium carcinogenesis. Mutation Research/ Fundamental and Molecular Mechanisms of Mutagenesis. 2003; 533:107-20.

  • Ognjanovic BI, Pavlovic SC, Maletic SD, Zikic RV, Stajn AS. Protective influence of vitamin E on antioxidant defence system in blood of rats treated with cadmium. Physiol. Res. 2003; 52: 563-570.

  • Shaikh ZA, Vu TT, Zaman K. Oxidative stress as a mechanism of chronic cadmium-induced hepatotoxicity and renal toxicity and protection by antioxidants. Toxicol Appl Pharmacol 1999; 154: 256-63.

  • Waisberg M, Joseph P, Hale B, Beyersmann D. Molecular and cellular mechanisms of cadmium carcinogenesis. Toxicol 2003;192: 95-117.

  • Guilidori P, Galli-Kienle M, Catto E, Strementinoli G. Transmethylation, transsulfuration and aminopropylation reactions of S-adenosyl-l-methionine in vivo. J Biol Chem 1984; 259:4205–11

  • Lu SC. S-adenosylmethionine. Intl J Biochem & Cell Biol 2000; 32:391–5

  • Friedel HA, Goa KL, Benfield P. S-Adenosyl-l-methionine: a review of its therapeutic potential in liver dysfunction and affective disorders in relation to its physiological role in cell metabolism. Drugs 1989; 38:389-416.

  • Mato JM, Alvarez L, Ortiz P, Pajares MA. S-adenosylmethionine synthesis: Molecular mechanisms and clinical implications, Pharmacol. Ther. 1997; 73:265-80.

  • Sarkar S, Yadav P, Trivedi R, Bansal AK, Bhatnagar D. Cadmiuminduced lipid peroxidation and the status of the antioxidant system in rat tissues. J Trace Elem Med Biol. 1995;9:144–9.

  • Ognjanovic BI, Markovic SD, Pavlovic SZ, Zikić RV, Stajn AS, Saicić ZS. Effect of chronic cadmium exposure on antioxidant defense system in some tissues of rats: protective effect of selenium. Physiol. Res. 2008; 57: 403–11.

  • Müller L. Consequences of cadmium toxicity in rat hepatocytes: mitochondrial dysfunction and lipid peroxidation. Toxicology 1986; 40: 285-95.

  • Klaassen CD, Liu J, Choudhuri S. Metallothionein: an intracellular protein to protect against cadmium toxicity. Annual review of pharmacology and toxicology 1999; 39: 267-94.

  • Gaurav D, Preet S, Dua KK. Chronic cadmium toxicity in rats: Treatment with combined administration of vitamins, amino acids, antioxidants and essential metals. J of Food and Drug Analysis 2011; 18 :464-70.

  • Lakshmi GD, Kumar PR, Bharavi K, Annapurna P, Rajendar B, Patel PT et al. Protective effect of Tribulus terrestris linn on liver and kidney in cadmium intoxicated rats. Indian J Exp Biol 2012; 50: 141-6.


Abstract Views: 465

PDF Views: 1




  • Protective Role of S-Adenosyl Methionine (SAMe) in Cadmium Induced Toxicopathological Changes in Wistar Rats

Abstract Views: 465  |  PDF Views: 1

Authors

Pratima Singh
Department of Pathology, College of Veterinary Science and Animal Husbandary, Duvasu, Mathura, India
A. K. Srivastava
Department of Pathology, College of Veterinary Science and Animal Husbandary, Duvasu, Mathura, India
Neeraj K. Gangwar
Department of Pathology, College of Veterinary Science and Animal Husbandary, Duvasu, Mathura, India
Shyama N. Prabhu
Department of Pathology, College of Veterinary Science and Animal Husbandary, Duvasu, Mathura, India
Raghavendra Yadav
Department of Pathology, College of Veterinary Science and Animal Husbandary, Duvasu, Mathura, India
Rahul Kumar
Department of Pathology, College of Veterinary Science and Animal Husbandary, Duvasu, Mathura, India

Abstract


Cadmium is considered to be one of the most toxic substances in the environment due to its wide range of organ toxicity and long elimination half-life. SAMe is recognized as the major methyl-donor for essential methylation reactions that occur in all living organisms. SAMe has been increasingly utilized as a therapeutic agent in liver and neurological disorders recently. The present study has been devised to explore the alleviating effects of SAMe in cadmium induced toxicopathological changes in rats. The rats were divided into four experimental groups: group I formed the control, group II animals were given cadmium chloride @ 200ppm in distilled water, orally, group III animals were given SAMe @ 1 mg/kg body weight, orally and group IV were given both CdCl2 and SAMe. Six rats from each group were humanely sacrificed at 30th, 60th and 90th day. The quantitative data of body weight, absolute organ weight, cadmium content and oxidative stress parameters was analyzed by Duncan's multiple range tests The group II animals showed most of the pathological changes compared to the rest of the group. The magnitude of lesions in various organs was lesser in group IV where SAMe was given. The severity of lesions increased with the advancement of experiment; most severe pathological changes occurring on the 90th day. The level of cadmium residue in liver and kidneys of rats was also found to be increasing with the time in group II and IV; with group IV showing a relatively lesser increase. Similarly the evaluation of oxidative stress parameters reflected the detrimental effect of cadmium in group II and an alleviating effect of SAMe in group IV. Based on the results obtained, SAMe is found to alleviate the toxicopathological effects of cadmium in rats which needs to be further explored.

Keywords


Cadmium, S-Adenosyl Methionine, Rats, Toxicopathology.

References





DOI: https://doi.org/10.22506/ti%2F2017%2Fv24%2Fi1%2F149036