Pharmacy and Drug Development

Abstract

Crude oil is a heterogeneous mixture of aliphatic hydrocarbons, aromatic hydrocarbons, including polycyclic aromatic hydrocarbons, resins, asphaltenes, and trace inorganic sulfur, nitrogen, and heavy metals. This study aimed to investigate the toxicological effects of consuming crude oil-contaminated catfish on hematological, serum electrolyte, and hepatic parameters in rats. Crude oil was used to contaminate juvenile catfish at concentrations of 0.1, 0.25, 0.5, and 1.0%. The contaminated fish were processed into feed and administered to rats over 30 days. Results demonstrated significant, dose-dependent adverse effects. Hematological analysis revealed a decline in hematocrit, red blood cells, hemoglobin, and mean corpuscular hemoglobin concentration (MCHC), alongside leukocytosis, indicating anemia and an inflammatory immune response. Serum electrolyte homeostasis was disrupted, marked by hypokalemia, hyponatremia, hypochloremia, and hypomagnesemia. Liver and kidney function were severely compromised, evidenced by elevated levels of bilirubin, urea, creatinine, and the activities of hepatic enzymes, including alanine aminotransferase (ALT) and aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), and acid phosphatase (ACP), coupled with reductions in total protein and albumin. The findings conclusively show that dietary exposure to crude oil-contaminated fish induces systemic toxicity, highlighting a significant public health risk for populations reliant on contaminated aquatic food sources and underscoring the urgent need for environmental remediation and continuous monitoring of petroleum pollutants.

Introduction

Crude is popular, if not the commonest, environmental pollutant in the niger Delta region of Nigeria [1,2]. Very few studies have been conducted on the effects of crude oil and petroleum products on hematological, histological, serum electrolyte levels, kidney function, and enzymatic/protein parameters [3]. Crude oil contamination of aquatic ecosystems is a pervasive environmental problem with far-reaching ecological, economic, and human-health consequences [4]. Oil spills, pipeline leaks, and routine petroleum industry discharges introduce complex mixtures of hydrocarbons, heavy metals, and other toxicants into rivers, estuaries, and coastal waters. These contaminants can persist in sediments and biota, entering food chains and undergoing bioaccumulation and biomagnification [5]. Fish, especially benthic and bottom-feeding species such as catfish, are particularly susceptible to exposure because of their feeding habits and close association with contaminated sediments. When contaminated fish are consumed by humans or other animals, the toxic constituents of crude oil may be transferred along the trophic ladder, potentially causing adverse biochemical, physiological, and pathological effects in consumers [6].

Crude oil is not a single compound but a heterogeneous mixture of thousands of organic molecules, including aliphatic hydrocarbons, aromatic hydrocarbons, including polycyclic aromatic hydrocarbons (PAHs), resins, asphaltenes, and trace inorganic constituents such as sulfur, nitrogen, and heavy metals [7-10]. Among these, low- and high-molecular-weight PAHs and certain heavy metals such as lead, cadmium, nickel, and vanadium are especially relevant toxicants because of their persistence, capacity to bioaccumulate, and well-documented genotoxic, hepatotoxic, and immunotoxic properties [11]. Mechanistically, components of crude oil can induce oxidative stress through the generation of reactive oxygen species (ROS), disrupt membrane integrity, interfere with enzyme systems, and form DNA adducts [12,13]. Hepatic metabolism of PAHs and other hydrocarbons frequently involves activation by cytochrome P450 enzymes to reactive intermediates that can cause lipid peroxidation, protein modification, and cellular injury [14]. These molecular and cellular insults commonly manifest as alterations in blood parameters, serum electrolytes, liver and kidney function markers, and changes in relevant enzymatic activities [15].

Bioaccumulation is the net uptake and retention of a chemical by an organism from all sources (water, sediment, and diet). Catfish (Clariidae, Clupeidae) often feed on benthic organisms and detritus, putting them in frequent contact with contaminated sediments where oil-derived compounds concentrate [6]. Catfish also have lipid-rich tissues that readily partition hydrophobic hydrocarbons, making them efficient accumulators of PAHs and other lipophilic constituents. Consequently, catfish harvested from polluted waters can carry significant contaminant burdens that pose a risk to predators and human consumers [16,17]. Investigating the toxic effects of catfish contaminated by crude oil is therefore ecologically and public-health relevant, especially in regions where catfish form a staple protein source.

Toxicants in crude oil can perturb multiple physiological systems; measuring a suite of hematological and biochemical parameters offers sensitive indicators of systemic toxicity and organ-specific damage [18]. Hematological indices such as hematocrit, red blood cell count (RBC), hemoglobin concentration, white blood cell count (WBC), and Mean Corpuscular Hemoglobin Concentration (MCHC) reflect oxygen-carrying capacity, erythropoiesis, and immune status. Decreases in hematocrit, RBC, or hemoglobin may indicate hemolysis, impaired erythropoiesis, or nutritional deficits secondary to toxic exposure; conversely, changes in WBC can reflect immunomodulation or inflammatory responses [19]. Serum electrolytes, sodium, potassium, chloride, and magnesium are fundamental to acid–base balance, osmotic regulation, and neuromuscular function [20]. Disruption of electrolyte homeostasis can be a downstream consequence of renal impairment, endocrine disturbance, or shifts in cellular permeability caused by toxicants [21].  Metabolic markers such as total protein, albumin, and bilirubin provide insight into hepatic synthetic function and biliary excretion, while renal function is typically assessed via serum urea and creatinine. Elevations in urea and creatinine often signal impaired glomerular filtration or tubular dysfunction [22].

Liver enzymes are central biomarkers for assessing hepatocellular injury and cholestasis [23]. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are predominantly cytosolic enzymes released into circulation when hepatocytes are damaged. Alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT) are more closely associated with cholestasis and biliary tract injury, while acid phosphatase (ACP) can reflect lysosomal perturbation and is sometimes used in toxicology as an index of cellular damage (Limdi & [24]. Changes in the activities of these enzymes in response to dietary crude oil exposure can therefore map the extent and nature of hepatic dysfunction induced by the contaminants. Therefore, toxicological outcomes commonly scale with exposure dose and duration, with low-level exposures producing subclinical or adaptive responses while higher concentrations can cause overt pathology [25]. The present work adopts a gradient of crude oil concentrations in contaminated catfish diets to define dose-dependent effects on hematological, biochemical, and enzymatic parameters in rats. Such a design enables identification of thresholds for biological effect, characterization of response curves, and potential identification of no-observed-adverse-effect levels (NOAEL) relevant for risk assessment [26].

The study aims to evaluate how crude oil-contaminated fish diets affect rats’ hematological parameters, hematocrit, red blood cells (RBC), hemoglobin, white blood cells (WBC), Mean Corpuscular Hemoglobin Concentration (MCHC), assess changes in serum sodium, potassium, chloride, and magnesium electrolyte levels, examine impacts on key metabolites; total protein, bilirubin, albumin, urea, creatinine and liver enzymes; alanine aminotransaminase (ALT), alkaline phosphatase (ALP), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), and average total acid phosphatase (ACP), and determine the dose-dependent effects of different crude oil concentrations, 0.1, 0.25, 0.5, and 1.0% on these hematological, biochemical, and physiological outcomes.

Materials and Methods

Materials

Crude oil, rats, healthy juvenile fish, plastic aquaria (30L), fishmeal (5g), EDTA tubes, Plain bottles, Universal bottles, Sucrose (500 g), Sodium Kit, Potassium Kit, Chloride Kit, Magnesium kit, Total protein kit, Total bilirubin Kit, Albumin Kit, Urea Kit, Creatinine Kit, enzyme assay kits (ALT, AST, AL, GGT, ACP), borehole water (to dilute crude oil and prepare concentrations: 0.1%, 0.25%, 0.5%, 1.0%), cylinders and pipettes, water quality testing kits (monitor pH, temperature, dissolved oxygen, and ammonia levels in the aquaria), aeration pumps (maintain adequate oxygen levels in the aquaria), weighing scale, oven, grinding machine, mortar and pestle (processing dried catfish into powder), rat feed pellets, mixing bowls and spatula, animal cages, chloroform, sterile surgical blades, centrifuge, Pasteur pipettes, Ice-cold and chips, 0.25 M sucrose solution, spectrophotometer for analyzing serum and liver homogenate samples, hematology analyzer to quantify hematological parameters - hematocrit, RBC, WBC, hemoglobin, MCHC, electrolyte analyzer to measure serum electrolyte levels - sodium, potassium, chloride, magnesium, and Biuret reagent to quantify total protein in liver homogenate.

Methods

Crude oil was obtained and diluted with borehole water and prepared in 0.1, 0.25, 0.5, and 1.0% concentrations, respectively. 150 healthy juvenile catfish were obtained and acclimatized for 10 days. The fish were divided into 6 groups (20 per group) and kept in 30 L plastic aquaria. The group to serve as control with catfish was cultured in borehole water, while 2-6 were exposed to the different concentrations of crude oil as stated above (properly labeled), and fed with ad libitum commercial fishmeal for 30 hours. The catfish were harvested after 30 hours, oven-dried at 40 °C, and processed as the diet for the rats. The diet for each group was mixed manually into rat feed pellets. Sixty rats were obtained from the animal house of the Department of Pharmacology, Niger Delta University, and were grouped into 6 (10 per group), with group one serving as the control. At the same time, 2-6 were given the formulated feeds of different crude oil concentrations (well labeled) for 30 days, after 10 days of acclimatization.  The rats were anesthetized in a jar by soaking in chloroform. Blood samples were collected by cutting the jugular vein with a sharp blade into well-labeled EDT tubes, spinning at 4000 rpm for 35 minutes in a centrifuge, and serum was collected using a Pasteur pipette for enzyme assay. The rats were then dissected, and the liver excised, placed in a 0.25M sucrose ice-cold solution. A known weight of the liver was cut, chopped into small pieces, and homogenized using a pre-cooled mortar and pestle in a bowl of ice chips. The homogenized tissue was diluted with 0.25M sucrose solution to obtain 1:5 dilutions for the enzyme assay.

The blood samples were analyzed numerically and histologically to quantify the effects of crude on some hematological parameters, including hematocrit, red blood cells, hemoglobin, white blood cells, and mean cellular hemoglobin concentration, compared with the standard group. The serum/plasma obtained was assessed to quantify the actual concentration of crude present in each sample. Other parameters, such as Sodium Na+, Potassium K+, Chloride Cl-, and Magnesium Mg2+ levels, respectively, were also assessed.

The total protein, bilirubin, albumin, urea, and creatinine content of the liver homogenate were determined using the Biuret method. The activities of alanine aminotransaminase (ALT), alkaline phosphatase (ALP), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), and average total acid phosphatase (ACP) were assessed, respectively.

Data Analysis

All data were analyzed using GraphPad Prism Statistical software utilizing One-Way and Welch’s ANOVA test. A p-value of <0.05 between the treatment and control group was considered statistically significant. All tests were conducted in triplicate.

Results

The results showed a clear dose-dependent decline in red blood cell parameters and a rise in white blood cells, indicating anemia and immune activation. Furthermore, significant disruptions in serum electrolytes, liver function markers, and elevated liver enzyme activities were observed, confirming multi-organ toxicity. The results are presented in tabular form for clarity and ease of interpretation. The data are divided into sections based on the parameters measured.

Hematological Parameters

An increasing effect of crude oil concentration (0–1.0%) on several hematological parameters was observed. As crude oil concentration rises, there was a progressive decrease in hematocrit, red blood cell count, hemoglobin levels, and MCHC, with statistically significant reductions observed at 0.5% and 1.0%. Conversely, white blood cell count increases significantly at higher crude oil concentrations, suggesting a possible inflammatory or immune response.

Figure 1:  Hematological parameters

(A) Hematocrit, P-value = 0.006. (B) Red Blood Cells, P-value = 0.006. (C) Hemoglobin, P-value = 0.003. (D) White Blood Cells, P-value = 0.04.  (E) mean corpuscular hemoglobin concentration, P-value = 0.03. Welch’s ANOVA test; *Significant difference (p < 0.05) compared to control. Mean ± SD.

Table 1 shows the effect of increasing crude oil concentration (0–1.0%) on serum electrolyte levels. Sodium, chloride, and magnesium concentrations decrease progressively with rising crude oil exposure, with significant reductions observed from 0.25% onwards. In contrast, potassium levels increase significantly starting at 0.25%, suggesting possible cellular damage or impaired renal regulation of electrolytes.

Table 1: Serum electrolyte levels in rats 

*Significant difference (p < 0.05) compared to control.

Figure 2 illustrates the impact of increasing crude oil concentration (0–1.0%) on serum biochemistry. Total protein and albumin levels decrease progressively, showing significant reductions from 0.25% onward, indicating impaired liver protein synthesis. In contrast, bilirubin, urea, and creatinine levels rise significantly with increasing crude oil exposure, suggesting hepatocellular dysfunction and compromised renal clearance.

Figure 2: Liver function parameters.

(A) Total protein, P-value = 0.05. (B) Bilirubin, P-value = 0.05. (C) Albumin, P-value = 0.07. (D) Urea, P-value = 0.008. (E) Creatinine, P-value = 0.005. Welch’s ANOVA test; *Significant difference (p < 0.05) compared to control.

Figure 3 shows that increasing crude oil concentration (0–1.0%) leads to a progressive and significant elevation of liver enzymes, including ALT, AST, ALP, GGT, and ACP, with significant increases observed from 0.25% onward. These findings indicate dose-dependent hepatocellular injury and cholestatic effects, consistent with liver damage caused by crude oil exposure.

Figure 3: Liver enzymes.

(A) Alanine aminotransferase (ALT), P-value = 0.007. (B) Aspartate aminotransferase (AST), P-value = 0.004. (C) Alkaline phosphatase (ALP), P-value = 0.008. (D) gamma-glutamyl transferase (GGT), P-value = 0.004. (E) Acid phosphatase (ACP), P-value = 0.05. Welch’s ANOVA test; *Significant difference (p < 0.05) compared to control.

Discussion

Crude oil exposure caused significant hematological changes, including anemia and immune activation. Serum electrolyte imbalances were observed, indicating potential renal dysfunction. Liver and kidney functions were impaired, as evidenced by elevated liver enzymes and metabolic waste products. The effects were dose-dependent, with higher crude oil concentrations causing more severe toxicity. This is similar to a previous report, where crude exposure was shown to negatively affect the ocular cavities among the oil-producing communities in the Niger Delta [27]. The study underscores the need for monitoring and mitigating crude oil pollution in aquatic ecosystems to protect both aquatic life and human health. The findings of this study provide compelling evidence for the systemic toxicity induced by consuming crude oil-contaminated fish. The observed hematological alterations are a primary indicator of hemotoxic effects. The dose-dependent decreases in hematocrit, RBC count, hemoglobin, and MCHC are strongly suggestive of a normocytic, normochromic anemia. This could result from direct hemolysis caused by hydrocarbon-induced oxidative damage to erythrocyte membranes or from suppressed erythropoiesis in the bone marrow due to the toxic burden. The concurrent significant increase in white blood cell count across treatment groups, particularly at higher concentrations (0.5% and 1.0%), points to a systemic inflammatory response or immunostimulation as the organism attempts to counteract the xenobiotic insult.

The hematological parameters results indicate a dose-dependent decrease in hematocrit, red blood cells, hemoglobin, and mean cellular hemoglobin concentration (MCHC), while white blood cells increased. This suggests that crude oil exposure may cause anemia and immune system activation. For the serum electrolytes, sodium, chloride, and magnesium levels decreased significantly, while potassium levels increased. This imbalance may indicate renal dysfunction or electrolyte dysregulation due to crude oil toxicity.

The significant perturbations in serum electrolyte levels reveal another critical facet of crude oil toxicity. The decreases in sodium, chloride, and magnesium levels, contrasted with an increase in potassium, are classic indicators of renal tubular dysfunction. Toxicants can damage the renal tubules, impairing their reabsorption capabilities for these essential ions. The rising potassium levels (hyperkalemia) are particularly concerning as they can disrupt cardiac electrophysiology. This electrolyte imbalance, likely compounded by hepatic damage affecting albumin synthesis and oncotic pressure, suggests a multi-organ failure scenario where renal and hepatic systems are simultaneously compromised.

The live functions test was also conducted. Elevated bilirubin, urea, and creatinine levels, along with decreased total protein and albumin, suggest impaired liver and kidney function. The increased activity of liver enzymes (ALT, AST, ALP, GGT, ACP) further confirms hepatic damage. The liver function parameters and enzyme activities offer the most direct evidence of organ-specific damage. The significant elevation in all measured liver enzymes (ALT, AST, ALP, GGT, ACP) is a hallmark of hepatocellular injury and cholestasis. The rise in ALT and AST, primarily cytosolic enzymes, indicates rupture of hepatocyte membranes and necrosis. The increased ALP and GGT activities are more associated with biliary epithelial damage and impaired bile flow. The dose-dependent increase in ACP activity further suggests lysosomal membrane destabilization and cellular degradation. This extensive hepatic damage is corroborated by the metabolic markers: decreased synthesis of total protein and albumin reflects impaired synthetic liver function, while the elevated levels of bilirubin, urea, and creatinine indicate a failure in the liver's detoxification and excretory roles and a consequent decline in glomerular filtration rate in the kidneys. The strong dose-response relationship for every parameter measured not only confirms the causality of crude oil exposure but also allows for the potential identification of a threshold for adverse effects, which appears to lie between the 0.1% and 0.25% exposure groups for many parameters.

Conclusion

Exposure to increasing crude oil concentrations (0–1.0%) caused dose-dependent hematological, biochemical, electrolyte, and enzymatic alterations. Hematocrit, red blood cell count, hemoglobin, MCHC, total protein, and albumin levels decreased progressively, suggesting anemia and impaired liver synthetic function. In contrast, white blood cell count, potassium, bilirubin, urea, and creatinine increased significantly, reflecting inflammatory response, electrolyte imbalance, hepatocellular damage, and renal dysfunction. Sodium, chloride, and magnesium levels declined, indicating disturbed electrolyte homeostasis. Additionally, ALT, AST, ALP, GGT, and ACP activities were significantly elevated, demonstrating dose-related hepatocellular injury and possible cholestasis. This study reveals that consuming catfish contaminated with crude oil leads to pronounced, dose-dependent toxic effects in rats, characterized by hemolytic anemia, disrupted electrolyte balance, and marked liver and kidney damage. The findings highlight the serious risk petroleum pollution poses to aquatic ecosystems and the food web. Contaminated seafood serves as a conduit for toxic hydrocarbons, facilitating their transfer to higher trophic levels, including humans. These results carry significant public health implications, especially for populations in oil-producing areas such as the Niger Delta region of Nigeria, where fish and other aquatic species are key components of the diet.

Acknowledgment

The authors sincerely appreciate the Nigeria Tertiary Education Trust Fund (TETFund) for providing financial support in conducting this research and publication. The authors also appreciate the Department of Pharmacology, Bayelsa Medical University.

References

1. Chinedu, Enegide, and Chukwuma Kelechukwu Chukwuemeka. "Oil spillage and heavy metals toxicity risk in the Niger Delta, Nigeria." Journal of Health and Pollution 8, no. 19 (2018): 180905.
   View at Publisher | View at Google Scholar
2. Anyanwu, Ihuoma N., Sebastian Beggel, Francis D. Sikoki, Eric O. Okuku, John-Paul Unyimadu, and Juergen Geist. "Pollution of the Niger Delta with total petroleum hydrocarbons, heavy metals and nutrients in relation to seasonal dynamics." Scientific Reports 13, no. 1 (2023): 14079.
   View at Publisher | View at Google Scholar
3. Fedan, Jeffrey S., Janet A. Thompson, Tina M. Sager, Jenny R. Roberts, Pius Joseph, Kristine Krajnak, Hong Kan, Krishnan Sriram, Lisa M. Weatherly, and Stacey E. Anderson. "Toxicological Effects of Inhaled Crude Oil Vapor." Current environmental health reports 11, no. 1 (2024): 18-29.
   View at Publisher | View at Google Scholar
4. Wei, Ying, Yukun Zhu, Liqun Yang, Chen Chen, Ming Yue, Zhuxin Mao, Yuchao Wang et al. "Effects of oil pollution on the growth and rhizosphere microbial community of Calamagrostis epigejos." Scientific Reports 15, no. 1 (2025): 1278.
   View at Publisher | View at Google Scholar
5. Sam, Kabari, Nenibarini Zabbey, Ijeoma Favour Vincent-Akpu, Gentle Komi, Peter Oghogho Onyagbodor, and Bolaji Bernard Babatunde. "Socio-economic baseline for oil-impacted communities in Ogoniland: towards a restoration framework in Niger Delta, Nigeria." Environmental Science and Pollution Research 31, no. 17 (2024): 25671-25687.
   View at Publisher | View at Google Scholar
6. Sharma, Babita, Puja Kumari, and M. Kumar. "Food and feeding habits of walking catfish, Clarias batrachus, and other commercial fish: A review." Tech. Int. J. Eng. Res 10 (2023): 879-889.
   View at Publisher | View at Google Scholar
7. Bunu, Samuel J., Benjamin U. Ebeshi, Hilda F. Kpun, Adesegun J. Kashimawo, Edebi N. Vaikosen, and Chubiyojo B. Itodo. "Atomic absorption spectroscopic (AAS) analysis of heavy metals and health risks assessment of some common energy drinks." Pharmacology and Toxicology of Natural Medicines (ISSN: 2756-6838) 3, no. 1 (2023): 1-10.
   View at Publisher | View at Google Scholar
8. BUNU, SAMUEL J., DORATHY GEORGE, D. E. G. H. I. N. M. O. T. E. I. ALFRED-UGBENBO, and BENJAMIN U. EBESHI. "Heavy metals quantification and correlative carcinogenic-risks evaluation in selected energy drinks sold in Bayelsa state using atomic absorption spectroscopic technique." International Journal of Chemistry Research (2023): 1-4.
   View at Publisher | View at Google Scholar
9. Jovita, Onyeukwu Nkechi, Urua Scholastica Patrick, Awala Victoria Ebisindor, Bunu Samuel Jacob, Onwuka Ngozi, and Osom Unwana Akpan Amanda. "Heavy Metals Health-Risk Assessment of Zingiber officinale in Akwa Ibom and Enugu following High Consumption During the COVID-19 Era." (2025).
   View at Publisher | View at Google Scholar
10. Jovita, Onyeukwu Nkechi, Okonkwo Ogochukwu Emmanuel, Osom Unwana Akpan, Anah Victor Udoh, and Bunu Samuel Jacob. "Health-Risk Assessment of Heavy Metals in Drinking Water Obtained from Public Primary Schools in Akwa Ibom State, Nigeria." Sch Acad J Pharm 3 (2025): 42-50.
    View at Publisher | View at Google Scholar
11. Jakubczyk, Karolina, Karolina Dec, Justyna Kałduńska, Dorota Kawczuga, Joanna Kochman, and Katarzyna Janda. "Reactive oxygen species-sources, functions, oxidative damage." Polski Merkuriusz Lekarski: Organ Polskiego Towarzystwa Lekarskiego 48, no. 284 (2020): 124-127.
    View at Publisher | View at Google Scholar
12. Skrypnik, Liubov, Pavel Maslennikov, Anastasia Novikova, and Mikhail Kozhikin. "Effect of crude oil on growth, oxidative stress and response of antioxidative system of two rye (Secale cereale L.) varieties." Plants 10, no. 1 (2021): 157.
    View at Publisher | View at Google Scholar
13. Smith, Jordan N., Kari A. Gaither, and Paritosh Pande. "Competitive metabolism of polycyclic aromatic hydrocarbons (PAHs): an assessment using in vitro metabolism and physiologically based pharmacokinetic (PBPK) modeling." International Journal of Environmental Research and Public Health 19, no. 14 (2022): 8266.
    View at Publisher | View at Google Scholar
14. Carter, Caitlyn Mara. "Alterations in blood components." Comprehensive toxicology (2017): 249.
    View at Publisher | View at Google Scholar
15. Dawood, Mahmoud AO, Ahmed E. Noreldin, and Hani Sewilam. "Blood biochemical variables, antioxidative status, and histological features of intestinal, gill, and liver tissues of African catfish (Clarias gariepinus) exposed to high salinity and high-temperature stress." Environmental Science and Pollution Research 29, no. 37 (2022): 56357-56369.
    View at Publisher | View at Google Scholar
16. Segaran, Thirukanthan Chandra, Mohamad Nor Azra, Rumeaida Mat Piah, Fathurrahman Lananan, Guillermo Téllez-Isaías, Huan Gao, Donald Torsabo, Zulhisyam Abdul Kari, and Noordiyana Mat Noordin. "Catfishes: A global review of the literature." Heliyon 9, no. 9 (2023).
    View at Publisher | View at Google Scholar
17. Sriram, Krishnan, Gary X. Lin, Amy M. Jefferson, Walter McKinney, Mark C. Jackson, Jared L. Cumpston, James B. Cumpston, Howard D. Leonard, Michael L. Kashon, and Jeffrey S. Fedan. "Biological effects of inhaled crude oil vapor V. Altered biogenic amine neurotransmitters and neural protein expression." Toxicology and applied pharmacology 449 (2022): 116137.
    View at Publisher | View at Google Scholar
18. Yavorkovsky, Leonid L. "Mean corpuscular volume, hematocrit and polycythemia." Hematology 26, no. 1 (2021): 881-884.
    View at Publisher | View at Google Scholar
19. Seifter, Julian L. "Body fluid compartments, cell membrane ion transport, electrolyte concentrations, and acid-base balance." In Seminars in nephrology, vol. 39, no. 4, pp. 368-379. WB Saunders, 2019.
    View at Publisher | View at Google Scholar
20. SRIVASTAVA, VISHNU K., HARSHVARDHAN ARYA, SARVAJIT S. UPPAL, BHIMBADHAR RATH, and NONICA LAISRAM. "Comparison of oral and intravenous rehydration among hospitalized children with acute diarrhoea." Journal of diarrhoeal diseases research (1985): 92-95.
    View at Publisher | View at Google Scholar
21. Kalas, M. Ammar, Luis Chavez, Monica Leon, Pahnwat Tonya Taweesedt, and Salim Surani. "Abnormal liver enzymes: A review for clinicians." World journal of hepatology 13, no. 11 (2021): 1688.
    View at Publisher | View at Google Scholar
22. Thakur, Simran, Vishal Kumar, Rina Das, Vishal Sharma, and Dinesh Kumar Mehta. "Biomarkers of hepatic toxicity: an overview." Current Therapeutic Research 100 (2024): 100737.
    View at Publisher | View at Google Scholar
23. Limdi, J. K., and G. M. Hyde. "Evaluation of abnormal liver function tests." Postgraduate medical journal 79, no. 932 (2003): 307-312.
    View at Publisher | View at Google Scholar
24. Attia, Youssef A., Mohammed A. Al-Harthi, and Hayam M. Abo El-Maaty. "The effects of different oil sources on performance, digestive enzymes, carcass traits, biochemical, immunological, antioxidant, and morphometric responses of broiler chicks." Frontiers in Veterinary Science 7 (2020): 181.
    View at Publisher | View at Google Scholar
25. Faboya, Oluwabamise L., Samuel O. Sojinu, and Joseph O. Otugboyega. "Preliminary investigation of polycyclic aromatic hydrocarbons (PAHs) concentration, compositional pattern, and ecological risk in crude oil-impacted soil from Niger delta, Nigeria." Heliyon 9, no. 4 (2023).
    View at Publisher | View at Google Scholar
26. Onyeukwu, Nkechi J., Samuel J. Bunu, Tologbonse A. Adedoyin, and Ngozi A. Onwuka. "Comparative Analysis of Petrochemicals Effects on Ocular Cavity: Prevalence and Pharmaceutical Interventions in the Niger Delta, Nigeria." Mathews Journal of Pharmaceutical Science 7, no. 2 (2023): 1-16.
    View at Publisher | View at Google Scholar