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 Table of Contents  
ORIGINAL ARTICLE
Year : 2018  |  Volume : 2  |  Issue : 2  |  Page : 142-145

Vitamin E supplementation and renal functions in acute celphos poisoning


1 Department of Biochemistry, Government Medical College, Agartala, Tripura
2 Department of Biochemistry, Pt. B. D. Sharma University of Health Sciences, Rohtak, Haryana, India

Date of Web Publication14-Jun-2018

Correspondence Address:
Dr. Simmi Kharb
#1396, Sector-1, Rohtak, Haryana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/bbrj.bbrj_14_18

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  Abstract 


Background: The present study was designed to evaluate the effects of vitamin E on phostoxin-induced changes in renal biochemical parameters in rats. Methods: Thirty disease free albino rats were selected to study the effect of acute aluminum phosphide poisoning (ALP poisoning) were further divided into 3 subgroups of ten each: A, B and C. Group A consists of rats given vehicle (Ginni Oil) only. Group B consists of rats given 5 ml “Celphos'mixture” (or 0.3mg/g body wt.). Group C consists of rats with acute Celphos poisoning along with Vitamin E (1.5 mg Vitamin E/g body weight of rat). Result: Mean serum creatinine concentration was significantly increased in both group B and group C as compared to group A. There is decrease in mean serum creatinine levels in acute ALP poisoning after vitamin E supplementation (group C) as compared to acute aluminium phosphide poisoning (group B), although this difference was not statistically significant. The rats were administered the doses via an infant feeding tube No. 8 and blood was obtained by Cardiac puncture one hour after feeding the dose. Serum Urea, serum creatinine and superoxide levels were estimated. The superoxide levels (nitroblue tetrazolium [NBT] reduction) were estimated. Mean serum urea concentration was significantly increased in both group B and group C as compared to group A. There is decrease in mean serum urea levels in acute ALP poisoning after vitamin E supplementation (group C) as compared to acute ALP poisoning (group B), although this difference was not statistically significant. NBT reduction was significantly increased in Group B as compared to Group A. Administration of Vitamin E to rats of Group C resulted in significant decrease of NBT reduction. Conclusion: Findings of the present study showed that Vitamin E via its antioxidant action and anti-inflamatory effects has protective effect on phosphine-induced toxicity in rats.

Keywords: Celphos, malondialdehyde, rats, renal function, vitamin


How to cite this article:
Biwas C, Bala J, Kharb S. Vitamin E supplementation and renal functions in acute celphos poisoning. Biomed Biotechnol Res J 2018;2:142-5

How to cite this URL:
Biwas C, Bala J, Kharb S. Vitamin E supplementation and renal functions in acute celphos poisoning. Biomed Biotechnol Res J [serial online] 2018 [cited 2021 Apr 17];2:142-5. Available from: https://www.bmbtrj.org/text.asp?2018/2/2/142/234450




  Introduction Top


Aluminum phosphide (ALP) is most commonly used solid fumigant and ideal pesticide since 1940. It is cheap, most efficacious, easy to use, and freely available in India (as Alphos, Celphos, Quickphos, Phostek, Phosfume, and Synfume) in the form of chalky white or brown 3 gm. Tablet contains 56% of ALP and 44% of ammonium carbonate.[1],[2] Studies had reported increased incidence of poisoning cases and deaths by acute ALP poisoning in suburban and rural parts of Northern India.[2]

ALP when comes in contact with hydrochloric acid or water in the stomach releases phosphine gas. This phosphine gas is colorless and extremely toxic and releases fishy or garlic-like odor.[3] The ingestion or inhalation of ALP has multisystem involvement, including gastrointestinal, respiratory, cardiovascular, musculoskeletal, central nervous, and urinary system.[3],[4],[5]

Nakaita et al. found that oxygen uptake in isolated rat liver mitochondria is inhibited by ALP. It inhibits ADP uncoupler and ion stimulated respiration, but exact target site was not identified. In a later detailed study, it was found to be strong inhibitor of mitochondrial respiration in active state than in resting state in mouse liver. It was found to inhibit uncoupled site and ion pumping state affecting pyruvate, malate, succinate, glycerophosphate, and ascorbate cytochrome substrates. This inhibition could not be reversed by uncouplers, suggesting that it is due to direct effect on electron transport which is an important electrochemical link between respiration and phosphorylation in mitochondria. The spectral and dichroism studies revealed an interaction with hememoeity of cytochrome oxidase (cytochrome-C) but are yet to be determined whether it interacts with either cytochrome a or a3 or both.[6] The result suggests that inhibition of cytochrome oxidase disturbs electron transport, leading to impaired energy metabolism.[7],[8]

Inhalation is the major route of phosphine toxicity.[9] Phosphine causes myocardial contractility and fluid loss which results in pulmonary edema. Hence, metabolic acidosis or mixed metabolic acidosis, respiratory alkalosis, and acute renal failure may also occur.[9],[10] Kidney is one of the major targets of phosphine poisoning in the human body. It has been suggested that phosphine that causes oxidative stress might be related to its nephrotoxic effect.[11]

Studies have shown recently that aluminum has been reported to accelerate oxidative damage to biomolecules such as lipid, protein, and nucleic acids.[12] Vitamin E is an important lipid-soluble chain-breaking antioxidant, preventing lipid peroxidation in membrane system.[13],[14] Vitamin E deficiency results in increased rate of lipid and protein oxidation, destruction of membrane function, and inactivation of membrane enzymes and receptors.[15] Ability of Vitamin E to ameliorate or inhibit the action of phostoxin could be due to removing the ROS via very rapid electron transfer chain that inhibits lipid peroxidation.[16] The decreased Vitamin E levels results in increased rate of lipid and protein peroxidation, destruction of membrane function, and inactivation of membrane enzymes and receptors. Hence, Vitamin E has received attention in diseases which are associated with excess free radical production.[13] The aim of the present study was to evaluate the effects of Vitamin E on phostoxin-induced changes in renal biochemical parameters.


  Methods Top


Disease-free albino rats of both sexes from the Departmental Animal Room of Medical College Rohtak fed on “Gold Mohur rat feed” were enrolled in study. During the entire period of the study, all the rats were caged separately. During the study, all the rats were handled as per the “guiding principles for research involving animals and human beings” under the “Recommendations from the Declaration of Helsinki” and “Guiding principles in the care and use of animals” as approved by the council of American Physiological Society.

The present study was done on 30 disease-free albino rats weighing 125–250 g of both sexes to study acute Celphos poisoning. The group for study on acute toxicity was further divided into three subgroups: A, B, and C. Each subgroup consists of 10 rats.

  • Group A – Rats dosed with vehicle (Ginni oil) only acting as control – 5 ml of prepared Ginni oil was given
  • Group B – Rats dosed with acute Celphos poisoning – 5 ml Celphos “mixture” (or 0.3 mg/g body weight)
  • Group C – Rats dosed with acute Celphos poisoning along with Vitamin E (1.5 mg Vitamin E/g body weight of rat.


The rats were administered the doses via an infant feeding tube No. 8 and the blood was obtained by cardiac puncture 1 h after feeding the dose. Serum urea levels were estimated by a modification of the procedure as described by Chaney and Marbach (DAM method). Serum creatinine was estimated by Jaffe's reaction as described by Brod and Sirota. Superoxide levels were estimated by a slightly modified method as described by Baehner and Nathan (nitroblue tetrazolium [NBT]). The malondialdehyde levels were estimated by modified method (thiobarbituric acid method) of Placer et al.


  Results Top


Mean serum urea concentration was significantly increased (P < 0.001) in both Group B and Group C (59.4 ± 9.16 mg/dL and 57.0 ± 5.12 mg/dL, respectively) as compared to Group A (42.9 ± 6.29 mg/dL). There was decrease in mean serum urea levels in acute ALP poisoning after Vitamin E supplementation (Group C) as compared to acute ALP poisoning (Group B), although this difference was not statistically significant [Table 1].
Table 1: Serum urea concentration in different groups

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Mean serum creatinine concentration was significantly increased (P < 0.01) in both Group B and Group C (1.26 ± 0.44 mg/dL and 1.10 ± 0.39 mg/dL, respectively) as compared to Group A (0.65 ± 0.26 mg/dL). There is decrease in mean serum creatinine levels in acute ALP poisoning after Vitamin E supplementation (Group C) as compared to acute ALP poisoning (Group B), although this difference was not statistically significant [Table 2].
Table 2: Serum creatinine concentration in different groups

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NBT reduction was expressed as △OD/15 min/mL serum. NBT reduction was significantly increased in acute ALP poisoning group (Group B) as compared to the normal group (Group A) (0.45 ± 0.06 vs 0.19 ± 0.08); P < 0.001. Administration of Vitamin E to the rats of Group C resulted in significant decrease of NBT reduction compared to the Group B (P < 0.001).


  Discussion Top


The present study reported significantly increased mean serum urea concentration in both Group B and Group C (59.4 ± 9.16 mg/dL and 57.0 ± 5.12 mg/dL, respectively) as compared to Group A (42.9 ± 6.29 mg/dL) (P < 0.001). There is decrease in mean serum urea levels in acute ALP poisoning after Vitamin E supplementation (Group C) as compared to acute ALP poisoning (Group B), although this difference was not statistically significant.

ALP can increase lipid peroxidation rates. Al +3 interacts with cell membrane directly, whereas aluminium salts were shown to accelerate peroxidation of membrane lipids induced by Fe (II) salts. Al +3 ions produce a subtle rearrangement in the membrane structure that facilitated the oxidative action of iron. Effect of aluminium on lipid peroxidation in various tissues such as liver, kidney, testis, and brain of different animals was investigated and aluminium increased the rate of lipid peroxidation in some studies while these changes were not observed in some studies.[13]

Antioxidant reduces oxidative radical-induced reaction. Vitamin E inhibits peroxidation of membrane lipids by scavenging lipid peroxyl radical with formation of tocopheroxyl radical.[16] Vitamin E counteracts aluminum harmful effects not only by preventing free radical formation but also by favoring aluminum disposal.[17]

Mean serum creatinine concentration was significantly increased (P < 0.01) in both Group B and Group C (1.26 ± 0.44 mg/dL and 1.10 ± 0.39 mg/dL, respectively) as compared to Group A (0.65 ± 0.26mg/dL). There is decrease in mean serum creatinine levels in acute ALP poisoning after Vitamin E supplementation (Group C) as compared to acute ALP poisoning (Group B), although this difference was not statistically significant.

Increased serum blood urea nitrogen has been detected indicating renal injury.[18] Newton et al. showed increased in kidney weights and coagulative necrosis of the tubular of the tubular epithelium in the outer cortex in some rats with pronounced effect in females compared to males.[19] It has been suggested that phosphine-induced oxidative stress can be responsible for its nephrotoxic effects.[11]

Kidney of phostoxin-treated rats showed marked deleterious histological changes.[20] The kidney section showed significant glomerular and tubular degeneration varying from glomerular basement thickening, interstitial inflammation, interlobular vessel disorder, tubular cell swelling, medullary vascular congestion, and moderate-to-severe necrosis.[21]

The results of our study are in agreement with other studies which also reported significant difference in serum urea and creatinine in experimental groups and controls.[22],[23] The increase in blood urea and creatinine in ALP poisoning is in agreement with the results of Yousef et al. in human.[24] Newton reported dose-dependent changes in blood urea, nitrogen, and other clinical parameters that were seen across exposed group.[25] In the control group, the blood serum level of these biochemical parameters showed normal levels, while the group that was exposed to phostoxin and Vitamin E showed variation in blood serum level of the parameter depending on the exposure time of the phostoxin and Vitamin E administered.[21]

Findings of the present study regarding reduction in NBT reduction (superoxide generation) following Vitamin E supplementation in rats give support to the concept that oxidative stress is induced by phosphine poisoning and possibly ALP toxicity causes disproportionate production of free radicals in tissue. The findings of the present study clearly indicate that Vitamin E is capable of preventing the deleterious effects of Al +3 ions in the treatment of acute ALP poisoning.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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Koreti S, Verma YS, Prasad N, Patel GS, Rajpur N. Aluminum phosphide poisoning in children-challenges in diagnosis and management. Sch Acad J Biosci 2014;2:505-9.  Back to cited text no. 1
    
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Turgut G, Enli Y, Kaptanoglu B, Turgut S, Genc O. Changes in the levels of MDA and GSH in mice serum, liver and spleen after aluminium administration. East J Med 2006;11:7-12.  Back to cited text no. 13
    
14.
Horváth ME, Faux SP, Smith AG, Blázovics A, van der Looij M, Fehér J, et al. Vitamin E protects against iron-hexachlorobenzene induced porphyria and formation of 8-hydroxydeoxyguanosine in the liver of C57BL/10ScSn mice. Toxicol Lett 2001;122:97-102.  Back to cited text no. 14
    
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Packer L. Protective role of Vitamin E in biological systems. Am J Clin Nutr 1991;53:1050S-5S.  Back to cited text no. 15
    
16.
Hussein MS, Abd-El-Rahman AH, Mohamed ET. The protective effect of Vitamin E against the neurotoxic effect of aluminum cholorid in male albino rat. J Am Sci 2010;6:978-1003.  Back to cited text no. 16
    
17.
Gonzalez MA, Alvarez Mdel L, Pisani GB, Bernal CA, Roma MG, Carrillo MC, et al. Involvement of oxidative stress in the impairment in biliary secretory function induced by intraperitoneal administration of aluminum to rats. Biol Trace Elem Res 2007;116:329-48.  Back to cited text no. 17
    
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Shakeri S, Mehrpour O. Aluminum phosphide poisoning in animals. Int J Med Toxicol Forensic Med 2015;5:81-97.  Back to cited text no. 18
    
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Newton PE, Schroeder RE, Sullivan JB, Busey WM. Inhalation toxicity of phosphine in rat: Acute, subchronic and developmental. Inhal Toxicol 1993;5:223-39.  Back to cited text no. 19
    
20.
Shadnia S, Sasanian G, Allami P, Hosseini A, Ranjbar A, Amini-Shirazi N, et al. A retrospective 7-years study of aluminum phosphide poisoning in Tehran: Opportunities for prevention. Hum Exp Toxicol 2009;28:209-13.  Back to cited text no. 20
    
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Saleki S, Ardalan FA, Javidan-Nejad A. Liver histopathology of fatal phosphine poisoning. Forensic Sci Int 2007;166:190-3.  Back to cited text no. 21
    
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Lall SB, Peshin SS, Mitra S. Methemoglobinemia in aluminium phosphide poisoning in rats. Indian J Exp Biol 2000;38:95-7.  Back to cited text no. 22
    
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Shadnia S, Soltaninejad K, Hassanian-Moghadam H, Sadeghi A, Rahimzadeh H, Zamani N, et al. Methemoglobinemia in aluminum phosphide poisoning. Hum Exp Toxicol 2011;30:250-3.  Back to cited text no. 23
    
24.
Yousef MI, Soliman NF, El-Demerdash FM. Aluminium phosphide-induced hepato-toxicity and oxidative damage in rats: The protective effect of α-lipoic acid. Open Conf Proc J 2015;6:18-23.  Back to cited text no. 24
    
25.
Newton PE. Inhalation toxicity of phosphine in the rat, acute sub-chronic and developmental intal. Toxicology 1993;5:223-39.  Back to cited text no. 25
    



 
 
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  [Table 1], [Table 2]



 

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