Journal of Toxicology

Journal of Toxicology / 2014 / Article

Research Article | Open Access

Volume 2014 |Article ID 917608 | 7 pages |

Camel Milk Beneficial Effects on Treating Gentamicin Induced Alterations in Rats

Academic Editor: Margaret James
Received18 May 2014
Revised10 Nov 2014
Accepted10 Nov 2014
Published03 Dec 2014


The potential effect of camel milk (CM) against gentamicin (GM) induced biochemical changes in the rat serum was evaluated. Four groups of six albino rats were used for control, CM fed, injected with GM(i.p.), and then fed and injected with GM. The results showed that the administration of GM significantly altered the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) activity in rat serum. CM restored these parameters to almost their normal range in group IV. Additionally, the present study showed that injection of rats with gentamicin caused an increase in malondialdehyde (MDA) and myeloperoxidase (MPO) activity while the antioxidant enzymes like superoxide dismutase (SOD) and glutathione s-transferase (GST) activity decreased significantly (). Administration of CM significantly () inhibited the formation of MDA and activity of MPO and upregulated the antioxidant enzymes (SOD and GST) activity. The overall findings of this study demonstrated that pretreatment with CM gave protection against GM induced hepatic damage possibly by inhibiting oxidative stress and inflammation, and hence camel milk can be identified as a new therapeutic agent.

1. Introduction

The unique characteristics of CM are seen in it is often used to counter diseases such as diabetes and hepatic and microbial infections [13], in addition to the reported improvement effects in blood and renal and hepatic functions [4]. Low in cholesterol, sugar, and protein but having higher levels of minerals as electrolytes, vitamins, and insulin, CM is presented as unique compared to the milk of other ruminant mammals [5]. Some active CM proteins were successfully studied, with specific antibacterial and antiviral promising results [1, 6, 7]. Insulin dependent diabetes patients could reduce their insulin dose by one third when taking raw CM [810], which refers to some control on metabolic and autoimmune diseases. In this field, autoimmune diseases, diabetes, and respiratory and various types of tuberculosis were extensively studied [11], in addition to specific hepatic intoxication studies [1217].

Aminoglycoside group of antibiotics, which include gentamicin (GM), have beneficial treatment effects against most of the life-threatening Gram-negative microorganisms [18], though their side effects encompass considerable nephrotoxic and hepatotoxic complications that were contracted by almost one third of the treated patients [19], especially in the GM nephrotoxic alterations field [20, 21]. In the present study, the major objectives were to evaluate the effect of CM consumption on GM induced biochemical changes in experimental rats by measuring the serum activity and levels of lipid peroxidation (MDA), MPO, GST, SOD, AST, ALT, ALP, and LDH.

2. Materials and Methods

2.1. Camel Milk

Camel milk was collected from local suburbs by hand milking. The samples were collected in sterile screw bottles and kept in cool boxes until transported to the laboratory. The rats were given this fresh milk (5 mL/rat/day) as such without any further treatment.

2.2. Animals

A total of 24 male albino rats (200–250 g) were obtained from animal house facility in the Research Center, Prince Sultan Military Medical City (PSMMC), Riyadh, Saudi Arabia. Rats were acclimated for ten days before starting the experiment. All animals were housed in standard cages (six rats/cage), feeding with standard laboratory diet and water ad libitum. The experimental animals were housed in air-conditioned rooms at 21–23°C and 60–65% of relative humidity and kept on a 12 h light/12 h dark cycle. The animals received humane care in accordance with the Guide for the Care and Use of Laboratory Animals, published by Ethics of Scientific Research Committee of PSMMC.

2.3. Gentamicin

80 mg (2 mL vials) gentamicin was obtained from Parkin Remedies.

2.4. Experimental Design

Animals were divided into four groups of six rats each. Group I served as control and received only normal saline injections (0.2 mL, i.p.). Group II was given CM only (5 mL/rat/day for fifteen days, orally). Group III was injected with GM (2 mL vials) only (80 mg/kg b.wt for the last ten days, i.p.). Group IV was given CM (alone for first five days) and then injected with GM (for 10 days).

2.5. Collection of Blood Serum

At the end of the experiment, that is, on day sixteen, the overnight fasted animals (the control and experimental animals) were sacrificed under mild ether anesthesia. Blood samples were collected by cardiac puncture before incision of the abdomen; 5 mL of blood samples was collected in plain tubes and serum was separated and frozen at −80°C until the time of analysis.

2.6. Biochemical Analysis

Commercial diagnostic kits (United Diagnostic Industry, UDI, Dammam, Saudi Arabia) were used for determination of ALT, AST, ALP, and LDH. Concentration of the biochemical constituents was calculated according to the manufacturer instructions.

2.7. Estimation of MDA

The concentration of thiobarbituric acid reactive substances (TBARS) was determined by the method of Ohkawa et al. [22]. In brief, the reaction mixture contained 0.1 mL of serum, 0.2 mL of sodium dodecylsulfate, 1.5 mL of acetic acid, and 1.5 mL of aqueous solution of TBA. The pH of 20% acetic acid was preadjusted with 1 M NaOH to 3.5. The mixture was made up to 4 mL with distilled water and heated at 95°C for 1 h, in a water bath. After cooling, 1 mL of distilled water and 5 mL of mixture of n-butanol and pyridine (15 : 1) were added and mixture was shaken vigorously on a vortex mixer. The absorbance of the upper organic layer was read at 532 nm using UV-VIS spectrophotometer.

2.8. Determination of Glutathione S-Transferase (GST) Activity

The method of Habig et al. [23] was used with some modifications to estimate the activity of glutathione s-transferase (GST). In a final volume of 2 mL, the reaction mixture consisted of 0.1 mole phosphate buffer, 1 mM reduced glutathione, 1 mM 1-chloro-2,4-dinitrobenzene (CDNB), and serum. The GST activity determined as nM CDNB conjugate formed min/ml using a molar extinction coefficient of 9.6 × 103 M−1 cm−1.

2.9. Determination of Superoxide Dismutase (SOD) Activity

Superoxide dismutase (SOD) activity was determined according to the method described by S. Marklund and G. Marklund [24]. The reaction mixture consisted of 0.5 mL of tris-buffer (50 mM; pH-8.2), 0.5 mL pyrogallol (0.5 mM), and 0.5 mL EDTA (1 mM), in different volumes, 0.025 mL, 0.05 mL, 0.075 mL, and 0.1 mL of serum. The change in absorbance was recorded at 420 nm. Activity was reported by its ability to inhibit 50% reduction of pyrogallol and the result is expressed as U/mL.

2.10. Determination of Myeloperoxidase (MPO)

The activity of the inflammatory marker myeloperoxidase (MPO) in the serum was measured with some modification according to the method of Barone et al. [25]. MPO in the serum was assayed by mixing 0.1 mL of serum with 2.9 mL of 50 mM potassium phosphate buffer (pH 6.0) containing 0.167 mg/mL o-dianisidinedihydrochloride (Sigma) and 0.0005% hydrogen peroxide (ICN Pharmaceuticals, Irvine, CA). The change in absorbance at 460 nm was measured for 3 min by using a UV-visible spectrophotometer (UV-160A, Shimadzu, Japan). MPO is expressed in units of activity per mL of serum, with 1 unit being the quantity of enzyme able to convert 1 μmol of hydrogen peroxide to water in 1 min at room temperature.

2.11. Statistical Analysis

Results were expressed as means ± standard error of mean (SEM). The significance of differences was calculated by SPSS program (version 20) using Student’s -test; was considered statistically significant.

3. Results

3.1. Effect of Camel Milk and Gentamicin on Biochemical Enzyme Levels

The activity of ALT, AST, ALP, and LDH was estimated in serum samples as the liver function biomarkers. These results are given in Table 1. The GM treatment markedly affected the liver specific enzymes. A significant increase was found in serums ALT, AST, ALP, and LDH activity in GM treated group as compared to control group ( to (); to (); to (); to (), resp.). This result suggests that these hepatic biomarkers were elevated in the serum due to release of the enzymes from damaged liver. However, a significant decrease was observed in the respective serum activity of above mentioned biomarkers of rats in group IV as compared to group III ( to ; to (); to (); to ()).

ParametersGroup I
Group II
Group III
Group IV
(CM + GM)

ALT (U/L)29.15 ± 1.8531.65 ± 0.9039.70 ± 2.17a33.62 ± 3.0b
AST (U/L)77.08 ± 2.568.37 ± 3.53d128.63 ± 6.31a111.02 ± 5.25a,b,c
ALP (U/L)58.80 ± 6.9077.07 ± 10.75d123.29 ± 9.09a87.29 ± 5.96a,b,c
LDH (U/L)332.89 ± 17.59212.04 ± 17.80d466.93 ± 15.54a398.81 ± 15.76a,b,c

Values are given as means ± SEM for groups of six animals each. Values are statistically significant between two groups ≤ 0.05. aControl group compared with gentamicin group; bcontrol groups compared with camel milk and gentamicin group; cgentamicin groups compared with camel milk and gentamicin group; dcontrol groups compared with camel milk group.
3.2. Effect of Camel Milk and Gentamicin on Lipid Peroxidation

Camel milk inhibited lipid peroxidation caused by GM administration in terms of MDA, a well-known biomarker of oxidative stress. Administration of GM led to a significant elevation in the level of MDA in group III compared to controls (). Administration with CM in group IV was significantly () effective in amelioration of MDA formation as compared to group III. There was no significant change observed in the level of MDA between controls and CM-treated animals (Figure 1).

3.3. Effect of Camel Milk and Gentamicin on Antioxidant Enzymes

The effect of CM administration on GM induced depletion in the activity of SOD and GST enzymes was examined and the results were shown in Figures 2 and 3, respectively. We have observed that there was a significant (,  ) depletion in the activity of these antioxidant enzymes in group III as compared to controls. However, CM administration in group IV significantly restored the activity of antioxidant enzymes when compared with group III (, ). There was no significant difference observed between groups I and II (Figures 2 and 3).

3.4. Effect of Camel Milk and Gentamicin on Myeloperoxidase Activity

We have observed that there was a significant increase in the activity of MPO in only GM treated group III as compared to group I (). However, CM administration in group IV significantly restored the activity of MPO when compared with group III (). There was no significant difference observed between groups I and II (Figure 4).

4. Discussion

The serum hepatic biomarkers, AST and ALT, activity were increased significantly in rats injected with GM in group III as compared to controls (group I), which suggest the release of enzymes of the damaged hepatocytes. These cytoplasmic enzymes released in the circulation were suggested to be acting on the signal transduction pathways leading to membrane cellular permeability, according to previous reports [2628]. GM toxicity enhances oxidative stress and the so formed reactive oxygen species (ROS) that exhaust the countering antioxidant enzymes and biomolecules [2730], referring to further impaired pathway processes [31]. The significant increase in the LDH of GM injected rats compared to controls is also in agreement with previously published findings [3, 13]. It was seen that the MDA (lipid peroxidation marker) and inflammatory marker MPO activity were significantly increased, whilst the endogenous antioxidants GST and SOD were decreased. This finding is consistent with researchers’ reports that attribute the inactivation of enzymes to their cross-linking with MDA that lead to increased accumulation of superoxide free radicals inducing more lipid peroxidation [13, 16, 28, 30, 32, 33].

On the other hand, treatment with camel milk was found to suppress the increase of serums AST and ALT activity induced by GM treatment in rats. This finding implies that CM has the potential to repair and protect liver tissues to be affected by GM injection, through membrane stabilizing and leakage prevention of intracellular enzymes. It could be interpreted that the repair and healing process of hepatic parenchymal cells should lead to reversal of serum transaminase levels [34]. CM protective effects had been reported previously in some related topics [3, 17, 35, 36], which attribute the harmful hepatic effects restoration, back to normal physiology, to CM consumption that affects the regeneration or protection of hepatocyte membrane integrity [37].

The serum antioxidant system enzymes (GST and SOD) and inflammatory marker (MPO) were also restored to normal optimum levels with CM consumption, which was attributed to its high contents of antioxidant vitamins, minerals, other elements [30], several potential therapeutic effects [8, 9], and disease resistance [2, 3842]. Dysfunctional mitochondria are responsible for the production of excessive superoxides, which are substrates for the conversion to inflammatory biomarkers [43] that mediate for contraction of some diseases [4446].

Some minerals and vitamin availability (as the case of abundant CM) enhance SOD levels and, oppositely, lower levels would lead to depletion [47] and it was shown in this study that SOD levels were significantly increased after CM administration. The reports of Barbagallo et al. [48] and Virginia et al. [49] have stressed the indispensable links between glutathione and other antioxidants with minerals and vitamins.

GM induced complications had been worked on with antioxidants by several researchers [21, 50, 51]. In Islamic communities, CM health benefits are popular, as has been stated by the Prophet Mohammed (PBUH) more than 1400 years ago. Several previous studies had experimentally proved the beneficial effects of camel milk. Some components in cow milk that are responsible for allergies are not found in camel milk whose protein components (beta-casein) are different [52] and decisive in curing and preventing food allergies [53]. Hence, it is used as a therapeutic agent in several diseases and also as antimicrobial [5457] and antiviral remedy [57, 58]. In addition to that camel milk contains a number of compatible immunoglobulins compared with human ones [59]. With respect to insulin, camel milk contains higher levels than the contents of cow and buffalo milk [60]. Recent studies have reported CM as possessing several beneficial characteristics [9, 17, 61, 62] but still the exact mechanisms and active remediation effects of CM against GM induced tissue damage are not fully investigated.

5. Conclusion

The present findings show that administration of CM exerts significant hepatoprotective and nephroprotective effects in gentamicin-treated rats. Further investigations are required to explore exactly the mechanisms of action of CM against gentamicin-induced physiological changes. Finally, the present study identifies new areas of research for development of better therapeutic agents for liver, kidney dysfunction, and other diseases.

Conflict of Interests

The authors declare that there is no conflict of interests regarding the publication of this paper.


The authors are grateful to PSMMC for offering them the opportunity to do this experimental work. They feel thankful to Mr. Nasreddien M. Abdo Osman for his help in this study.


  1. E.-R. M. Redwan and A. Tabll, “Camel lactoferrin markedly inhibits hepatitis C virus genotype 4 infection of human peripheral blood leukocytes,” Journal of Immunoassay and Immunochemistry, vol. 28, no. 3, pp. 267–277, 2007. View at: Publisher Site | Google Scholar
  2. H. Saltanat, H. Li, Y. Xu, J. Wang, F. Liu, and X.-H. Geng, “The influences of camel milk on the immune response of chronic hepatitis B patients,” Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi, vol. 25, no. 5, pp. 431–433, 2009. View at: Google Scholar
  3. T. Althnaian, I. Albokhadaim, and S. M. El-Bahr, “Biochemical and histopathological study in rats intoxicated with carbontetrachloride and treated with camel milk,” SpringerPlus, vol. 2, article 57, 2013. View at: Publisher Site | Google Scholar
  4. T. S. Sharmanov, A. K. Zhangabylov, and R. D. Zhaksylykova, “Mechanism of the therapeutic action of whole mare's and camel's milk in chronic hepatitis,” Voprosy pitaniia, vol. 1, pp. 17–23, 1982. View at: Google Scholar
  5. K. H. Knoess, “Milk production of the dromedary,” in Proceeding of the IFS Symposium Camels (SC '79), pp. 201–214, Khartoum, Sudan, 1979. View at: Google Scholar
  6. C. Conesa, L. Sánchez, C. Rota et al., “Isolation of lactoferrin from milk of different species: calorimetric and antimicrobial studies,” Comparative Biochemistry and Physiology—B Biochemistry and Molecular Biology, vol. 150, no. 1, pp. 131–139, 2008. View at: Publisher Site | Google Scholar
  7. R. H. Omer and A. H. Eltinay, “Changes in chemical composition of camel's raw milk during storage,” Pakistan Journal of Nutrition, vol. 8, no. 5, pp. 607–610, 2009. View at: Publisher Site | Google Scholar
  8. R. P. Agrawal, S. C. Swami, R. Beniwal, D. K. Kochar, and R. P. Kothari, “Effect of camel milk on glycemic control, risk factors and diabetes quality of life in type-1 diabetes: a randomised prospective controlled study,” International Journal of Diabetes in Developing Countries, vol. 22, no. 2, pp. 70–74, 2002. View at: Google Scholar
  9. R. P. Agrawal, S. Budania, P. Sharma et al., “Zero prevalence of diabetes in camel milk consuming Raica community of north-west Rajasthan, India,” Diabetes Research and Clinical Practice, vol. 76, no. 2, pp. 290–296, 2007. View at: Publisher Site | Google Scholar
  10. R. H. Mohamad, Z. K. Zekry, H. A. Al-Mehdar et al., “Camel milk as an adjuvant therapy for the treatment of type 1 diabetes: verification of a traditional ethnomedical practice,” Journal of Medicinal Food, vol. 12, no. 2, pp. 461–465, 2009. View at: Publisher Site | Google Scholar
  11. M. B. Rao, R. C. Gupta, and N. N. Dastur, “Camels' milk and milk products,” Indian Journal of Dairy Science, vol. 23, pp. 71–78, 1970. View at: Google Scholar
  12. F. Al-Hashem, M. Dallak, N. Bashir et al., “Camel's milk protects against cadmium chloride induced toxicity in white albino rats,” The American Journal of Pharmacology and Toxicology, vol. 4, no. 3, pp. 107–117, 2009. View at: Publisher Site | Google Scholar
  13. F. Al-Hashem, “Camel's milk protects against aluminum chloride-induced normocytic normocromic anemia, lipid peroxidation and oxidative stress in erythrocytes of white albino rats,” American Journal of Biochemistry and Biotechnology, vol. 5, no. 3, pp. 127–136, 2009. View at: Publisher Site | Google Scholar
  14. M. Dallak, “Camel's milk protects against cadmium chloride-induced hypocromic microcytic anemia and oxidative stress in red blood cells of white albino rats,” American Journal of Pharmacology and Toxicology, vol. 4, no. 4, pp. 136–143, 2009. View at: Publisher Site | Google Scholar
  15. M. E. M. Afifi, “Effect of camel’s milk on cisplatin-induced nephrotoxicity in Swiss Albino mice,” The American Journal of Biochemistry and Biotechnology, vol. 6, pp. 141–147, 2010. View at: Google Scholar
  16. K. G. Al-Fartosi, O. S. Khuon, and I. Al-Tae, “Protective role of camel's milk against paracetamol induced hepatotoxicity in male rats,” International Journal of Research in Pharmaceutical and Biomedical Sciences, vol. 2, no. 4, pp. 1795–1799, 2011. View at: Google Scholar
  17. A. A. Khan and M. Al-zohairy, “Hepatoprotective effects of camel milk against CCl4-induced hepatotoxicity in rats,” Asian Journal of Biochemistry, vol. 6, no. 2, pp. 171–180, 2011. View at: Publisher Site | Google Scholar
  18. J. L. Ho and M. Barza, “Role of aminoglycoside antibiotics in the treatment of intra-abdominal infection,” Antimicrobial Agents and Chemotherapy, vol. 31, no. 4, pp. 485–491, 1987. View at: Publisher Site | Google Scholar
  19. S. Cuzzocrea, E. Mazzon, L. Dugo et al., “A role for superoxide in gentamicin-mediated nephropathy in rats,” European Journal of Pharmacology, vol. 450, no. 1, pp. 67–76, 2002. View at: Publisher Site | Google Scholar
  20. H. D. Humes, “Aminoglycoside nephrotoxicity,” Kidney International, vol. 33, no. 4, pp. 900–911, 1988. View at: Publisher Site | Google Scholar
  21. J. Pedraza-Chaverrí, A. E. González-Orozco, P. D. Maldonado, D. Barrera, O. N. Medina-Campos, and R. Hernández-Pando, “Diallyl disulfide ameliorates gentamicin-induced oxidative stress and nephropathy in rats,” European Journal of Pharmacology, vol. 473, no. 1, pp. 71–78, 2003. View at: Publisher Site | Google Scholar
  22. H. Ohkawa, N. Ohishi, and K. Yagi, “Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction,” Analytical Biochemistry, vol. 95, no. 2, pp. 351–358, 1979. View at: Publisher Site | Google Scholar
  23. W. H. Habig, M. J. Pabst, and W. B. Jakoby, “Glutathione S-transferases. The first enzymatic step in mercapturic acid formation,” The Journal of Biological Chemistry, vol. 249, no. 22, pp. 7130–7139, 1974. View at: Google Scholar
  24. S. Marklund and G. Marklund, “Involvement of the superoxide anion radical in the autoxidation of pyrogallol and a convenient assay for superoxide dismutase,” European Journal of Biochemistry, vol. 47, no. 3, pp. 469–474, 1974. View at: Publisher Site | Google Scholar
  25. F. C. Barone, L. M. Hillegass, W. J. Price et al., “Polymorphonuclear leukocyte infiltration into cerebral focal ischemic tissue: myeloperoxidase activity assay and histologic verification,” Journal of Neuroscience Research, vol. 29, no. 3, pp. 336–345, 1991. View at: Publisher Site | Google Scholar
  26. M. R. I. Khan, M. A. Islam, M. S. Hossain, M. Asadujjaman, M. I. I. Wahed, and B. M. Rahman, “Antidiabetic effects of the different fractions of ethanolic extracts of Ocimum sanctum in normal and alloxan induced diabetic rats,” Journal of Scientific Research, vol. 2, no. 1, pp. 158–168, 2010. View at: Google Scholar
  27. A. A. Noorani, K. A. Gupta, K. Bhadada, and M. K. Kale, “Protective effect of methanolic leaf extract of Caesalpinia bonduc (L.) on gentamicin-induced hepatotoxicity and nephrotoxicity in rats,” Iranian Journal of Pharmacology and Therapeutics, vol. 10, no. 1, pp. 21–25, 2011. View at: Google Scholar
  28. A. O. Ademiluyi, G. Oboh, T. R. Owoloye, and O. J. Agbebi, “Modulatory effects of dietary inclusion of garlic (Allium sativum) on gentamycin-induced hepatotoxicity and oxidative stress in rats,” Asian Pacific Journal of Tropical Biomedicine, vol. 3, no. 6, pp. 470–475, 2013. View at: Publisher Site | Google Scholar
  29. T. Nakajima, A. Hishida, and A. Kato, “Mechanisms for protective effects of free radical scavengers on gentamicin-mediated nephropathy in rats,” The American Journal of Physiology—Renal Fluid and Electrolyte Physiology, vol. 266, no. 3, pp. F425–F431, 1994. View at: Google Scholar
  30. L. Y. Al-Ayadhi and N. E. Elamin, “Camel milk as a potential therapy as an antioxidant in autism spectrum disorder (ASD),” Evidence-Based Complementary and Alternative Medicine, vol. 2013, Article ID 602834, 8 pages, 2013. View at: Publisher Site | Google Scholar
  31. J. J. Klemens, R. P. Meech, L. F. Hughes, S. Somani, and K. C. M. Campbell, “Antioxidant enzyme levels inversely covary with hearing loss after amikacin treatment,” Journal of the American Academy of Audiology, vol. 14, no. 3, pp. 134–143, 2003. View at: Google Scholar
  32. E. B. Kurutas, A. Cetinkaya, E. Bulbuloglu, and B. Kantarceken, “Effects of antioxidant therapy on leukocyte myeloperoxidase and Cu/Zn-superoxide dismutase and plasma malondialdehyde levels in experimental colitis,” Mediators of Inflammation, vol. 2005, no. 6, pp. 390–394, 2005. View at: Publisher Site | Google Scholar
  33. I. Yaman and E. Balikci, “Protective effects of nigella sativa against gentamicin-induced nephrotoxicity in rats,” Experimental and Toxicologic Pathology, vol. 62, no. 2, pp. 183–190, 2010. View at: Publisher Site | Google Scholar
  34. M. I. Thabrew, P. D. T. M. Joice, and W. Rajatissa, “A comparative study of the efficacy of Pavetta indica and Osbeckia octandra in the treatment of liver dysfunction,” Planta Medica, vol. 53, no. 3, pp. 239–241, 1987. View at: Publisher Site | Google Scholar
  35. E. M. Hamad, E. A. Abdel-Rahim, and E. A. Romeih, “Beneficial effect of camel milk on liver and kidneys function in diabetic sprague-dawley rats,” International Journal of Dairy Science, vol. 6, no. 3, pp. 190–197, 2011. View at: Google Scholar
  36. K. G. Al-Fartosi, A. Majid, M. A. Auda et al., “The role of camel’s milk against some oxidant-antioxidant markers of male rats treated with CCl4,” International Journal of Research in Pharmaceutical and Biomedical Sciences, vol. 3, no. 1, pp. 385–389, 2012. View at: Google Scholar
  37. M. T. Boroushaki, E. Asadpour, H. R. Sadeghnia, and K. Dolati, “Effect of pomegranate seed oil against gentamicin-induced nephrotoxicity in rat,” Journal of Food Science and Technology, vol. 51, no. 11, pp. 3510–3514, 2014. View at: Publisher Site | Google Scholar
  38. R. Yagil, Camel Milk and Autoimmune Diseases: Historical Medicine, 2004.
  39. H. E. Mohamed, H. M. Mousa, and A. C. Beynen, “Ascorbic acid concentrations in milk from Sudanese camels,” Journal of Animal Physiology and Animal Nutrition, vol. 89, no. 1-2, pp. 35–37, 2005. View at: Publisher Site | Google Scholar
  40. O. Zafra, S. Fraile, C. Gutiérrez et al., “Monitoring biodegradative enzymes with nanobodies raised in Camelus dromedarius with mixtures of catabolic proteins,” Environmental Microbiology, vol. 13, no. 4, pp. 960–974, 2011. View at: Publisher Site | Google Scholar
  41. Y. Shabo and R. Yagil, “Etiology of autism and camel milk as therapy,” The Journal of Endocrine Genetics, vol. 4, no. 2, pp. 67–70, 2005. View at: Google Scholar
  42. A. I. Al-Humaid, H. M. Mousa, R. A. El-Mergawi, and A. M. Abdel-Salam, “Chemical composition and antioxidant activity of dates and dates-camel-milk mixtures as a protective meal against lipid peroxidation in rats,” American Journal of Food Technology, vol. 5, no. 1, pp. 22–30, 2010. View at: Publisher Site | Google Scholar
  43. S. Rose, S. Melnyk, O. Pavliv et al., “Evidence of oxidative damage and inflammation associated with low glutathione redox status in the autism brain,” Translational Psychiatry, vol. 2, article e134, 2012. View at: Publisher Site | Google Scholar
  44. R. M. Nagra, B. Becher, W. W. Tourtellotte et al., “Immunohistochemical and genetic evidence of myeloperoxidase involvement in multiple sclerosis,” Journal of Neuroimmunology, vol. 78, no. 1-2, pp. 97–107, 1997. View at: Publisher Site | Google Scholar
  45. P. S. Green, A. J. Mendez, J. S. Jacob et al., “Neuronal expression of myeloperoxidase is increased in Alzheimer's disease,” Journal of Neurochemistry, vol. 90, no. 3, pp. 724–733, 2004. View at: Publisher Site | Google Scholar
  46. A. K. Anthony, J. Russo, B. Jepson, and A. Wakefield, “Low serum myeloperoxidase in autistic children with gastrointestinal disease,” Journal of Clinical and Experimental Gastroenterology, vol. 2, no. 2, pp. 85–94, 2009. View at: Publisher Site | Google Scholar
  47. N. A. Meguid, A. A. Dardir, E. R. Abdel-Raouf, and A. Hashish, “Evaluation of oxidative stress in autism: defective antioxidant enzymes and increased lipid peroxidation,” Biological Trace Element Research, vol. 143, no. 1, pp. 58–65, 2011. View at: Publisher Site | Google Scholar
  48. M. Barbagallo, L. J. Dominguez, M. R. Tagliamonte, L. M. Resnick, and G. Paolisso, “Effects of vitamin E and glutathione on glucose metabolism: role of magnesium,” Hypertension, vol. 34, no. 4, pp. 1002–1006, 1999. View at: Publisher Site | Google Scholar
  49. M. Virginia, M. B. Smith, M. J. Brauner, and M. P. Majerus, “Glutathione synthesis in human erythrocytes,” The Journal of Clinical Investigation, vol. 50, pp. 507–513, 1971. View at: Google Scholar
  50. C. Yanagida, K. Ito, I. Komiya, and T. Horie, “Protective effect of fosfomycin on gentamicin-induced lipid peroxidation of rat renal tissue,” Chemico-Biological Interactions, vol. 148, no. 3, pp. 139–147, 2004. View at: Publisher Site | Google Scholar
  51. P. D. Maldonado, D. Barrera, I. Rivero et al., “Antioxidant S-allylcysteine prevents gentamicin-induced oxidative stress and renal damage,” Free Radical Biology and Medicine, vol. 35, no. 3, pp. 317–324, 2003. View at: Publisher Site | Google Scholar
  52. O. U. Beg, H. Von Bahr-Lindstrom, Z. H. Zaidi, and H. Jornvall, “A camel milk whey protein rich in half-cystine. Primary structure, assessment of variations, internal repeat patterns, and relationships with neurophysin and other active polypeptides,” European Journal of Biochemistry, vol. 159, no. 1, pp. 195–201, 1986. View at: Publisher Site | Google Scholar
  53. F. Martin, C. Volpari, C. Steinkühler et al., “Affinity selection of a camelized V(H) domain antibody inhibitor of hepatitis C virus NS3 protease,” Protein Engineering, vol. 10, no. 5, pp. 607–614, 1997. View at: Publisher Site | Google Scholar
  54. O. U. Beg, H. Von Bahr-Lindstrom, Z. H. Zaidi, and H. Jornvall, “Characterization of a camel milk protein rich in proline identifies a new β-casein fragment,” Regulatory Peptides, vol. 15, no. 1, pp. 55–62, 1986. View at: Publisher Site | Google Scholar
  55. R. Yagil, “Camel milk—a review,” International Journal of Animal Sciences, vol. 2, pp. 81–89, 1987. View at: Google Scholar
  56. E. K. Barbour, N. H. Nabbut, W. M. Ferisch, and H. M. Ai-Nakhli, “Inhibition of pathogenic bacteria by camels milk: relation to whey lysozyme and stage of lactation,” Journal of Food Protection, vol. 47, pp. 838–840, 1984. View at: Google Scholar
  57. E. I. El Agamy, R. Ruppanner, A. Ismail, C. P. Champagne, and R. Assaf, “Antibacterial and antiviral activity of camel milk protective proteins,” Journal of Dairy Research, vol. 59, no. 2, pp. 169–175, 1992. View at: Publisher Site | Google Scholar
  58. M. T. El-Mougi, Basic Pediatrics, Faculty of Medicine, Al-Azher University, Cairo, Egypt, 1999.
  59. E. Y. Mona, O. M. Ragia, A. K. H. Abeer, and T. E. Mosa, “Biochemical effects of fermented camel milk on diarrhea in rats,” New York Science Journal, vol. 3, no. 5, pp. 106–111, 2010. View at: Google Scholar
  60. E. M. Hamad, E. A. Abdel-Rahim, and E. A. Romeih, “Beneficial effect of camel milk on liver and kidneys function in diabetic Sprague-Dawley rats,” International Journal of Dairy Science, vol. 6, no. 3, pp. 190–197, 2011. View at: Google Scholar
  61. H. Tsuda and T. Miyamoto, “Angiotensin I-converting enzyme inhibitory peptides in skim milk fermented with Lactobacillus helveticus 130B4 from camel milk in Inner Mongolia, China,” Journal of the Science of Food and Agriculture, vol. 88, no. 15, pp. 2688–2692, 2008. View at: Publisher Site | Google Scholar
  62. A. A. Elayan, A. M. E. Sulieman, and F. A. Saleh, “The hypocholesterolemic effect of Gariss and Gariss containing bifidobacteria in rats fed on a cholesterol-enriched diet,” Asian Journal of Biochemistry, vol. 3, no. 1, pp. 43–47, 2008. View at: Publisher Site | Google Scholar

Copyright © 2014 Abdulrahman K. Al-Asmari et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1738 Views | 954 Downloads | 9 Citations
 PDF  Download Citation  Citation
 Download other formatsMore
 Order printed copiesOrder

We are committed to sharing findings related to COVID-19 as quickly and safely as possible. Any author submitting a COVID-19 paper should notify us at to ensure their research is fast-tracked and made available on a preprint server as soon as possible. We will be providing unlimited waivers of publication charges for accepted articles related to COVID-19.