Protective Effect of Camel Milk Against Gentamicin-Induced Acute Renal Damage in Experimental Rats

Hany Salah Mahmoud Azab1, Salah Mohamed El-Sayed2,3, Mohamed T. A. Soliman3,4, Alaa Abd Algwad5, Heba M.A. Abdelrazek6, Heba A. Alian7*

1Prophetic Medicine Association for Medical Sciences and Complementary Medicine, Qantara West Center, Ismailia, Egypt; 2Department of Basic Medical Sciences, Taibah Faculty of Medicine, Taibah University, Saudi Arabis. 42353, P.O. Box 344; 3Department of Medical Biochemistry, Faculty of Medicine, Sohag University, Egypt; 4Department of Medical Laboratory Sciences, College of Applied Medical Sciences, University of Bisha, Bisha 67614, Saudi Arabia; 5Department of Food Safety, Hygiene and Technology, Faculty of Veterinary Medicine, Suez Canal University, Egypt; 6Department of Physiology, Faculty of Veterinary Medicine, Suez Canal University, Egypt; 7Department of Nutrition and Clinical Nutrition, Faculty of Veterinary Medicine, Suez Canal University, Egypt.

Received | October 22, 2025; Accepted | December 01, 2025; Published | December 13, 2025

*Correspondence | Heba A. Alian, Department of Nutrition and Clinical Nutrition, Faculty of Veterinary Medicine, Suez Canal University, Egypt; Email: [email protected]

Citation | Azab HSM, SM El-Sayed, Soliman MTA, Algwad AA, Abdelrazek HM, Alian HA (2025). Protective effect of camel milk against gentamicin-induced acute renal damage in experimental rats. Adv. Anim. Vet. Sci., 13(s1):211-218.

DOI | https://dx.doi.org/10.17582/journal.aavs/2025/13.s1.211.218

ISSN (Online) | 2307-8316

Copyright: 2025 by the authors. Licensee ResearchersLinks Ltd, England, UK.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

INTRODUCTION

The aminoglycoside group of antibiotics, including gentamicin (GM), exhibits significant therapeutic efficacy against the majority of Gram-negative bacteria (Wang et al., 2022). However, their use is limited by substantial side effects, particularly nephrotoxic and hepatotoxic complications, which occur in nearly one-third of treated patients (Mert et al., 2025). The onset of renal failure caused by aminoglycosides is typically gradual, with a slower daily increase in serum creatinine compared to other forms of renal failure cases. Creatinine level and blood urea nitrogen generally begin to rise 7–10 days after the start of aminoglycoside medication. In more than half of nephrotoxic cases, the deterioration in kidney function becomes noticeable only after treatment has ended (Pazarci et al., 2024). Besides, aminoglycoside-induced toxicity is often associated with tubular dysfunction and several electrolyte imbalances (Hodges, 2019).

Camel milk (CM) has been traditionally consumed in desert communities and is valued in the folk medicine of several countries, including Saudi Arabia and Egypt (Abdelazez et al., 2024). Compared to milk from other animals, camel milk has lower levels of lactose and saturated fat, while being richer in protective proteins, including lysozyme and immunoglobulins (Almasri et al., 2024). Numerous studies have highlighted the therapeutic potential of CM, suggesting benefits for managing digestive disorders, diabetes, hepatitis C, and certain cancers (Khan et al., 2021). Moreover, it has established protective effects against heavy metal toxicity (e.g., lead and cadmium) and has been reported to enhance both liver and kidney functions (Vijiyakumar and Prince, 2024). The typical constituents of camel milk are 2.9–5.8% lactose, 2.5–4.5% protein, 2.9–5.5% fat, 0.35–0.90% ash, and 8.9–14.3% nonfat solids. It has a high concentration of vitamins, including A, E, C, and folate, besides minerals such as sodium, potassium, calcium, zinc, and chlorine (El‐Agamy, 2017). In Islamic populations, the health benefits of CM are widely recognized, as mentioned in the teachings of Prophet Mohammed (PBUH). Several investigations have established the valuable influences of camel milk. Certain components in cow milk that trigger allergies are absent in camel milk, which contains different protein components, specifically beta-casein (Hassanein, 2023), and are crucial in treating and avoiding food allergies (Pal et al., 2024). Besides, camel milk contains numerous immunoglobulins that are compatible with those found in human milk (Mirmiran et al., 2017). Therefore, it serves as a favorable agent in various disorders and functions as an antimicrobial.

Besides, camel milk is distinguished by its high concentration of antioxidants, including the potent antioxidant lactoferrin, as well as several antioxidant trace elements and vitamins (Arab et al., 2021). In addition, camel milk contains several bioactive proteins, such as nanoantibodies and the lactoperoxidase enzyme, which contribute to its notable antiviral, antibacterial, and immune-modulatory effects. Moreover, both clinical and experimental studies have demonstrated the beneficial effects of camel milk in diabetes mellitus, wound healing (Ebaid et al., 2015), and toxicant-induced renal pathologies (Arab et al., 2018).

Since oxidative stress and inflammation are central to the pathogenesis of gentamicin-induced renal injury, it is reasonable to hypothesize that the combined antioxidant and anti-inflammatory components of camel milk could mitigate these deleterious effects. Lactoferrin and α-lactalbumin may regulate apoptotic signaling pathways and inhibit inflammatory cytokine activation in the renal cortex, while the enzymatic antioxidants in camel milk may scavenge free radicals and reduce lipid peroxidation. Additionally, micro minerals may increase the activity of endogenous antioxidant systems like glutathione peroxidase, offering another defense against the oxidative burden caused by gentamicin. Therefore, this study aimed to evaluate the protective effect of camel milk against gentamicin-induced acute kidney damage in rats. Specifically, the research examined the biochemical, histopathological, and immunobiological changes in renal function following gentamicin administration. Also, this study seeks to provide experimental evidence supporting the therapeutic ability of camel milk as a native remedy for nephrotoxicity.

MATERIALS AND METHODS

Experimental material

Powdered camel milk was obtained from the Prophetic Medicine Association in Ismailia, Egypt. The chemical composition of the powdered camel milk was as follows: fat, 34.87%; carbohydrates, 33.79%; protein, 21.9%; moisture, 1.53%; total ash, 7.91%; and acid-insoluble ash, 0.033%. The analysis was conducted by the Egyptian Organization for Standardization and Quality (EOS). Commercially available camel milk powder (manufacturer specifications on a dry basis: total carbohydrates 33.79%, fats 34.87%, proteins 21.9% on a dry basis) was reconstituted in distilled water at a ratio of 1:3.9 (w/v) immediately before use. The reconstituted milk was used to ensure compositional consistency and stability throughout the experiment to mimic the composition of fresh camel milk. Gentamicin (10 mg/mL, 1 mL vials; Memphis Co. for Pharmaceutical and Chemical Industries, Cairo, Egypt) was used for experimental induction.

Experimental animals

Forty Wistar albino rats, 12 weeks of age and weighing ≈ 186.82 g, were utilized in this experiment. The animals were housed in polyethylene cages (ten rats per cage) under controlled conditions, with a temperature of 24 ± 2°C with 60–65% relative humidity, and natural daylight cycles. A standard laboratory diet (Table 1) was provided to the rats throughout the experimental period. The diet was formulated to satisfy the nutritional needs of rats according to (NRC, 1995) guidelines, along with clean water, were supplied ad libitum.

 

Table 1: Composition of standard laboratory diet.

Ingredients	Diet %
Poultry by-product meal (55 CP%)	21
Yellow corn	54
Fine wheat bran	8
Wheat flour	10
Vegetable oil	4
Lysine	0.313
Methionine	0.257
Premix *	2.31
Salt (NaCl)	0.12
Total	100.00
Calculated values
ME (Kcal/Kg)	3070.5
CP	18.1
Ca	0.60
P	0.40

 

* Each 3 kg of the vitamin–mineral premix contained the following components: Vitamin A (12,000 IU), Vitamin D₃ (2,000 IU), Vitamin E (1 g), Vitamin K₃ (1 g), Vitamin B₁ (1 g), Vitamin B₂ (5 g), Vitamin B₆ (1.5 g), Vitamin B₁₂ (10 mg), Biotin (50 mg), Pantothenic acid (10 g), Nicotinic acid (30 g), Folic acid (1 g), Manganese (60 g), Zinc (50 g), Iron (30 g), Copper (4 g), Iodine (300 mg), Selenium (100 mg), and Cobalt (100 mg). Calcium carbonate (CaCO₃) was used as the carrier to complete the 3 kg mixture. Vet Care Nutrition Co., Cairo, Egypt, supplied the premix.

 

The housing environment was kept quiet, hygienic, and free from cold stress to minimize discomfort and external disturbances. All animals were acclimatized for one week before the experiment began. Any sick animals were isolated and treated as necessary, and signs of distress were promptly addressed. To keep the material clean, the cages, food hoppers, and water bottles were cleaned at least once a week.

Experimental design

Forty adult Wistar rats were utilized in the experiment. The 1st group (T1) was administered saline (0.2 mL, intraperitoneally). The 2nd group (T2) was supplied with camel milk orally at a rate of 10 ml/kg body weight. The 3rd group (T3) administered gentamicin intraperitoneally at a dose of 100 mg/kg body weight to induce nephrotoxicity. The 4th group (T4) received camel milk (10 ml/kg, orally) and gentamicin (100 mg/kg, i.p.).

The timeline was as follows: all treatments were administered once daily for 14 consecutive days. Gentamicin was injected intraperitoneally, while camel milk was provided orally. Control groups were injected equivalent volume of saline. The protective group received camel milk one hour before gentamicin administration each day.

Sampling

At the end of the experimental period, blood samples were obtained from the retro-orbital plexus using light diethyl ether anesthesia and put into plain tubes. The samples underwent centrifugation at 4000 rpm for 10 minutes, after which the separated sera were stored at –20°C until the serum analysis was conducted. After serum collection, the rats were euthanized with an overdose of chloroform. Kidney tissue samples were collected and subjected to histopathological and immunohistochemical analyses. A separate section of the kidney tissue was rinsed with ice-cold PBS and homogenized at a rate of 100 mg/mL in cold Tris buffer with protease inhibitors. The homogenate underwent centrifugation at 10,000 × g for 10 minutes at 4 °C, after which the supernatant was gathered for analysis. The clarified lysate was utilized to assess oxidative stress biomarkers and pro-inflammatory cytokines.

Body weight measurements and relative kidney weight

Body weight (BW) was recorded weekly, and body weight gain (WG) was calculated as follows: WG (g) is estimated as the difference between the final body weight (g) and the initial body weight (g). The formula used for calculating relative kidney weight (RKW) in rats: relative kidney weight (g/100 g BW) = (kidney weight (g)/body weight (g)) ×100.

Serum analysis

Creatinine was measured kinetically using the method of Richard et al. (1974). Urea was calculated using the enzymatic colorimetric procedure of Gutmann and Bergmeyer (1974) while uric acid was assessed following the procedure of Liddle et al. (1959). By using commercial kits (Sunlong Biotech®, China). Kidney injury molecule-1 (KIM-1) was detected following the instructions of commercial ELISA kits (Rat KIM-1 ELISA kit from Cusabio®).

Oxidative stress and cytokines assay of the kidney homogenate

Lipid peroxidation was estimated via the determination of thiobarbituric acid reactive substances, specifically quantifying malondialdehyde (MDA), the final product of lipid peroxidation, at 534 nm (Ohkawa et al., 1979). The determination of reduced glutathione (GSH) was conducted through its reaction with dithio-bis-2-nitrobenzoic acid, following the methodology outlined by Woolliams et al. (1983). IL-6 and TNF-α concentrations were quantified using purchased available RAT ELISA kits (MyBioSource Co®, San Diego, CA 92195-3308, USA) following the manufacturer’s protocols.

Histopathological evaluation

Kidney specimens were gathered from all groups and fixed in 10% neutral buffered formalin, followed by dehydration in an ascending series of ethyl alcohol (70–100%). Tissue samples were prepared using standard techniques for Hematoxylin and Eosin stain (Bancroft, 2013).

Statistical analysis

Data are presented as mean±standard error (SE). Statistical analyses were done using SPSS software, version 21.0 (IBM Corp., NY, USA). One-way analysis of variance (ANOVA) was applied to compare means among experimental groups. Duncan’s multiple range test was employed as a post hoc analysis to detect specific group differences (Chambers et al., 2017). Statistical significance was stated as P < 0.05.

RESULTS

Body weight measurements and relative kidney weight

At the end of the experiment, rats in T1, T2, and T4 showed a non-significant increase in final body weight, while the gentamicin group (T3) exhibited a decrease in final body weight. Additionally, T1, T2, and T4 showed positive weight gain. In contrast, T3 demonstrated a significant loss in body weight gain (–14.50 g) (P < 0.05). No significant differences were found in relative kidney weight among the experimental groups (Table 2).

Kidney function parameters

Gentamicin (T3) caused pronounced kidney dysfunction, as proven by significant increases in all renal biomarkers. Serum creatinine levels were highest in T3 compared to other groups (P < 0.05). Co-treatment with camel milk (T4) significantly lowered creatinine levels compared to T3. Similarly, serum urea concentrations were significantly higher in the gentamicin group (T3). Uric acid levels were significantly elevated in T3, but were significantly reduced in T4 compared to T3 (P < 0.05). T4 significantly reduced KIM-1 levels to 0.41 pg/mL, a value like those in the control groups (T1 and T2), which had the lowest levels (Table 3).

Oxidative stress markers and cytokines assay

T3 showed a significant decline in GSH levels compared to T1 and T2 (P < 0.05). MDA was significantly increased in the gentamicin group (2.98 nmol/g) compared to other groups. T4 significantly reduced MDA levels to 1.61 nmol/g compared to T3. Regarding the inflammatory biomarkers, IL-6 concentrations were significantly higher in T3 (100.14 pg/g) (P < 0.05). T4 significantly lowered IL-6 to 65.67 pg/g (P < 0.05) compared to T3. For TNF-α, T3 showed the greatest significant value in comparison with T1 and T2, while T4 exhibited a slight reduction compared to T3.

 

Table 2: Body weight measurements and relative kidney weight of rats in different experimental groups.

Group
Parameter	T1	T2	T3	T4
Initial body wt. (g)	175.60a ± 15.8	189.25a± 17.79	187.25a ± 17.78	198.00a ± 11.23
Final body wt. (g)	196.40a ±13.90	200.75a ± 16.47	172.75a ±12.49	202.75a±10.88
Body weight gain (g)	20.80a± 5.37	11.50a± 2.32	-14.50b ± 7.71	4.75a ± 3.63
Relative kidney weight (g/100 g BW)	0.79a ± 0.23	0.63a ± 0.01	0.75a ± 0.03	0.63 a ± 0.009

 

Data are presented as mean ± SE. Means having different superscripts in the same row are significantly different (P < 0.05). T1: Normal saline injections (0.2 mL, i.p.). T2: Camel milk orally (10 ml/kg BW). T3: Gentamicin (100 mg/kg BW, i.p.). T4: Camel milk orally (10 ml/kg BW) + Gentamicin (100 mg/kg, i.p.).

 

Table 3: Serum biochemical markers of kidney function in different experimental groups.

Group
Parameter	T1	T2	T3	T4
Creatinine (mg/dl)	1.04c± 0.13	0.90c ± 0.05	3.42a ± 0.43	2.10 b ± 0.18
Urea (mg/dl)	28.64b ± 8.36	33.75ab ± 1.40	43.76a ± 2.26	37.90ab ± 1.04
Uric acid (mg/dl)	4.04c ± 0.25	3.87c ± 0.23	7.66a ± 0.75	6.03b ± 0.53
KIM-1 (pg/mL)	0.30b ± 0.03	0.26b ± 0.03	0.66a ± 0.09	0.41b ± 0.03

 

Data are presented as mean ± SE. Means having different superscripts in the same row are significantly different (P < 0.05). T1: Normal saline injections (0.2 mL, i.p.). T2: Camel milk orally (10 ml/kg BW). T3: Gentamicin (100 mg/kg BW, i.p.). T4: Camel milk orally (10 ml/kg BW) + Gentamicin (100 mg/kg, i.p.).

 

Table 4: Oxidative stress marker and cytokines assay in different experimental groups.

Group
Parameter	T1	T2	T3	T4
GSH (pg/g)	51.29a ± 4.30	49.85a ± 3.72	25.74b ± 2.54	34.43b ± 2.25
MDA (nmol/g)	1.05c ± 0.11	0.96c ± 0.07	2.98a ± 0.17	1.61b± 0.10
IL-6 (pg/g)	32.29c ± 4.89	31.29c ± 4.41	100.14a ± 4.53	65.67b ± 4.90
TNF alpha (pg/ g)	38.00b ± 7.63	37.30b ± 7.55	115.83a ± 22.21	82.41ab ±13.19

 

Both T1 and T2 had the lowest cytokine levels, confirming a normal inflammatory status (Table 4).

 

 

Histopathological evaluation

The light microscopy assessment of H&E-stained renal sections, obtained from both the control and CM groups, revealed a normal micromorphological architecture, comprising both renal cortical and medullary portions. Regarding the cortical tissue, it contained renal corpuscles and their tubular series, proximal and distal convoluted tubules. Meanwhile, the renal medulla consisted mainly of Henel’s loops and excretory duct system, collecting and papillary ducts. The renal corpuscle was composed of numerous loops of blood capillary (glomerulus) surrounded by a Bowman’s capsule. The tubular epithelial lining was of cuboidal to columnar types with prominent vesicular nuclei. While the medullary ductal epithelium was of columnar to transitional type (Figure 1). In contrast, the kidneys of rats in the gentamicin group (T3) showed marked histopathological changes in their kidneys, including shrunken glomeruli with wide subcapsular urinary spaces, vascular congestion of the inter-tubular capillaries, extravasated RBCs, and tubular degeneration. Such degenerative changes were indicated by dilatation of tubular lumens, tubular cell swelling, pyknotic nuclei, exfoliated and sloughed epithelial cells, epithelial lining fragmentation, along with interstitial inflammatory cells infiltration (Figure 1). Renal specimens obtained from rats of T4 group revealed mild renal variations and lesser damages when compared to T3 group, as well as exhibiting a marked alleviation and restoration of normal renal appearance (Figure 1).

DISCUSSION

This study evaluated the protective effects of camel milk against gentamicin-induced nephrotoxicity in experimental rats. The findings revealed that T3 exhibited an obvious loss in body weight gain. This reduction in weight gain may be due to the toxic effects of gentamicin, which is known to cause nephrotoxicity and disrupt normal metabolic functions, affecting growth and general health status (Gamaan et al., 2023). Gentamicin can cause gastrointestinal discomfort, malaise, and reduced food intake. Lower nutrient intake directly reduces body weight gain (Randjelovic et al., 2017). The protective effects of camel milk are likely due to its rich nutritional components, which decrease gentamicin-induced oxidative stress and kidney injury (Behrouz et al., 2022). By supporting metabolic stability and overall health, camel milk may help restore appetite and improve feed efficiency, thereby mitigating the decrease in body weight gain observed in the gentamicin group (T3). Although camel milk did not fully recover body weight gain to control levels. This discrepancy may be attributed to the persistent systemic metabolic stress induced by gentamicin, which is known to cause anorexia, dehydration, and reduced protein synthesis. While camel milk mitigated renal injury, it may not have completely reversed the overall metabolic burden or appetite suppression associated with nephrotoxicity. This finding strengthens the distinction between functional renal recovery and systemic growth restoration, emphasizing that the protective effects of camel milk are primarily renal and anti-inflammatory rather than anabolic. The lack of difference in relative kidney weights indicates that the treatments did not significantly affect kidney hypertrophy or atrophy based on the organ-to-body weight ratio.

Our results revealed that gentamicin caused significant renal dysfunction, as indicated by marked elevations in serum creatinine, urea, and uric acid levels. Treatment with camel milk markedly mitigated these nephrotoxic effects, leading to improved renal function and a significant reduction in serum biomarkers of kidney injury compared to the gentamicin-only group. However, it is important to note that in the camel milk-treated group (T4), the levels of creatinine and uric acid remained slightly higher than those of the control groups (T1/T2), suggesting that the protective effect of camel milk was partial rather than complete. Gentamicin is known to cause oxidative stress, tubular necrosis, and injury to glomerular function, leading to elevated levels of serum urea and creatinine (Gamaan et al., 2023). The camel milk attenuated these changes, indicating its ability to protect renal tissue structure and function. The protective role of camel milk may be attributed to its high content of antioxidant components, minerals, and vitamins (such as C, A, and E) that help recover cellular defense mechanisms (Almasri et al., 2024).

Kidney injury molecule-1 (KIM-1) is a chief sensitive and specific indicator for early detection of renal tubular damage. Its increased expression signals a compensatory response aimed at limiting apoptosis and supporting tubular cell restoration and re-epithelialization (Su et al., 2025). In our study, gentamicin administration caused a marked increase in serum KIM-1 levels, indicating significant tubular damage and impaired renal function. However, camel milk co-treatment in T4 significantly lowered KIM-1 levels, approaching the values of the control and camel milk groups (T1 and T2), both of which showed the lowest levels, reflecting its protective effect on renal tubular integrity. This decrease may be attributed to the antioxidant and anti-inflammatory properties of camel milk, which help suppress oxidative stress and cellular injury in renal tissues (Behrouz et al., 2022). These findings are consistent with reported studies on camel milk’s attenuation of diabetes mellitus (Raj et al., 2023) and gentamicin-induced nephrotoxicities (Al-Asmari et al., 2014a; Hamad et al., 2018). The observed decrease in KIM-1 levels further supports the histopathological findings, confirming that camel milk exerts a nephroprotective effect by preserving tubular architecture and preventing epithelial cell damage.

The oxidative stress markers confirmed a clear pattern of gentamicin-induced kidney injury and the protective impact of camel milk. Glutathione (GSH) is a tripeptide and a valuable non-enzymatic antioxidant that is crucial for the integrity of cells against oxidative stress (Hamad et al., 2018). Nephrotoxicity induced by GM is related to a reduction of serum levels of GSH due to the boost of lipid peroxides and reactive oxygen species (Hussain et al., 2012). Malondialdehyde (MDA) is considered an indicator of lipid peroxidation (Alharbi et al., 2017). Lower MDA levels protect renal cells from damage by gentamicin administration. Our data revealed that camel milk (T4) decreased lipid peroxidation, as demonstrated by a reduction in serum MDA levels. This lowering effect might be due to the natural antioxidant content, antioxidant enzymes, and free radical scavenging properties of camel milk. Recently, many reports stated that fermented camel milk had a high scavenging activity (Hamad et al., 2018). Also, camel milk lactoferrin was shown to have a high antioxidant activity (Habib et al., 2013). Similarly, several studies have reported that GM-induced complications can be ameliorated by antioxidants (Al-Asmari et al., 2014b; Pedraza-Chaverrı́ et al., 2003; Yanagida et al., 2004).

IL-6 and TNF-α concentrations were markedly elevated in T3, reflecting a strong inflammatory response. In contrast, there was a notable decline in T4, indicating that camel milk provided a marked anti-inflammatory amelioration. Both T1 and T2 groups had the lowest cytokine levels, proving a normal inflammatory status. Overall, gentamicin markedly boosted inflammation, while camel milk exerted a significant protective effect by reducing inflammatory mediators. As gentamicin administration is well known to trigger inflammatory responses that contribute to renal tissue damage, largely mediated by the upregulation of pro-inflammatory cytokines such as IL-6 and TNF-α (Gamaan et al., 2023). On the other hand, the protective effect of camel milk can be attributed to the bioactive components of camel milk, including vitamins and immunomodulatory proteins such as lactoferrin, which together inhibit the release of pro-inflammatory signals and protect renal cells from cytokine-induced damage (Al-Omari et al., 2019).

Histopathological examination of kidney tissues provided further evidence supporting the biochemical findings of this study. Kidneys from gentamicin-treated rats exhibited severe histological alterations, including shrunken glomeruli with wide subcapsular urinary spaces, vascular congestion of the inter-tubular capillaries, extravasated RBCs, and tubular degeneration, typical features of gentamicin-induced nephrotoxicity. In contrast, rats treated with camel milk demonstrated marked enhancement in renal histoarchitecture, characterized by nearly normal glomerular and tubular structures, minimal cellular degeneration, and reduced inflammatory infiltration. These histological improvements indicated that camel milk effectively preserved renal tissue integrity and mitigated gentamicin-induced morphological damage. The protective effect is likely attributed to the antioxidant, anti-inflammatory, and membrane-stabilizing properties of camel milk components, which prevent oxidative and inflammatory injury to renal cells (Abdelazez et al., 2024). So, the histopathological examinations strongly corroborate the biochemical and cytokine results, confirming the nephroprotective potential of powdered camel milk.

CONCLUSION AND RECOMMENDATIONS

Gentamicin adversely affected body weight gain, whereas camel milk mitigated this weight loss without altering relative kidney weight. Also, it induced significant renal dysfunction, evidenced by elevated serum creatinine, urea, uric acid, and KIM-1 levels, along with increased IL-6, TNF-α, and marked histopathological kidney damage. It was demonstrated that camel milk administration significantly improved renal function, reduced tubular injury, and attenuated inflammation in gentamicin-treated rats, demonstrating its effective nephroprotective potential. Therefore, we suggest that camel milk could be used as a natural supplement to mitigate the toxic effects of gentamicin therapy.

ACKNOWLEDGMENT

We would like to express our sincere thanks to Dr. Ahmed Shaker, Lecturer of Pathology, Faculty of Veterinary Medicine, Suez Canal University, for his valuable assistance in the histopathological assessment

NOVELTY STATEMENT

Our study provides new insights into the ameliorative role of camel milk against gentamicin-induced nephrotoxicity in rats. Unlike previous studies focusing primarily on the antioxidant properties of camel milk, this work provides a comprehensive assessment of its biochemical, immunological, and histopathological effects in mitigating renal injury. The conclusions highlight camel milk as a potential natural therapeutic agent for avoiding drug-induced kidney damage.

AUTHOR’S CONTRIBUTION

HA: Conceptualization, experimental design, data curation. SE-S: Methodology development, data validation, and supervision of analytical procedures. MS: Project administration, overall supervision, manuscript editing. AAA: Laboratory work, sample preparation, and technical support throughout experimentation. HA: Literature review, data organization, and critical revision of the manuscript. HA: Statistical analysis, interpretation of results, contribution to discussion and conclusions, and correspondence with the journal.

Generative AI and AI-assisted technology statement

The authors of this study affirm that no generative AI tools, such as text-to-image generators and large language models (such ChatGPT and Copilot), were used in any way during the preparation, writing, or editing of this publication.

Conflict of interest

The authors have declared no conflict of interest.

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