Kingsley Omage
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Kingsley Omage has a total of 60 co-authors. Here are the top co-authors by number of shared publications:
- Marshall Arebojie Azeke
Functional Foods and Nutraceutical Research Group Department of Biochemistry Faculty of Life Sciences Ambrose Alli University Edo Nigeria
12 shared publications - Sylvia Oghogho Omage
Department of Biochemistry, Faculty of Life Sciences, University of Benin, Benin City, Nigeria
10 shared publications - Aishat Mary Osagie
Department of Biochemistry, Faculty of Life Sciences, Ambrose Alli University, Ekpoma, Nigeria
4 shared publications Silvanus Olu Innih
Department of Anatomy, School of Basic Medical Sciences, College of Medical Sciences, University of Benin, Benin City, Nigeria
3 shared publications- Emmanuel Chukwuma Omenna
Https://dx.doi.org/54715Obafemi Awolowo University, Institute of Agricultural Research and Training, Ibadan, Oyo State, Nigeria
2 shared publications - James A. McCormick
Oregon Health and Science University
2 shared publications
Latest Publications
- Open Access
- 3 August 2026
- Published by Wiley in Food Chemistry International
Nutraceutical Benefits of Anchomanes difformis Rhizome and Its Effects on Blood Glucose and Hepatorenal Function in Normoglycemic Rats
This study aims to scientifically validate the nutraceutical profile, hypoglycemic efficacy, and preliminary safety profile of Anchomanes difformis dried rhizome powder and its extracts. We analyzed the dried rhizome powder, aqueous extracts, and ethanol extracts of A. difformis . Proximate analysis and qualitative phytochemical screening were carried out. Furthermore, blood glucose, liver enzymes, and kidney markers were evaluated in normal Wistar rats over a period of 21 days. Our results show that the rhizome contained 47.12% carbohydrate, 12.87% crude protein, phosphorus, potassium, and calcium. Phytochemical analysis detected phenols, tannins, flavonoids, saponins, glycosides, oxalates, phytates, and trypsin inhibitors. Both extracts lowered plasma glucose levels in a dose‐ and time‐dependent manner. Doses between 200 and 500 mg/kg were well tolerated. Chronic doses ≥ 1000 mg/kg induced hepatotoxicity, marked by elevated AST and ALP levels. High doses of the ethanol extract significantly increased urea levels. We conclude that A. difformis rhizomes possess appreciable nutritional and hypoglycemic properties that support their ethnomedicinal use. However, consumption must be carefully regulated due to dose‐dependent hepatic and renal toxicity during long‐term, high‐dose use.
- 3 August 2026
- Published by Wiley in Food Chemistry International
Open AccessNutraceutical Benefits of Anchomanes difformis Rhizome and Its Effects on Blood Glucose and Hepatorenal Function in Normoglycemic Rats
This study aims to scientifically validate the nutraceutical profile, hypoglycemic efficacy, and preliminary safety profile of Anchomanes difformis dried rhizome powder and its extracts. We analyzed the dried rhizome powder, aqueous extracts, and ethanol extracts of A. difformis . Proximate analysis and qualitative phytochemical screening were carried out. Furthermore, blood glucose, liver enzymes, and kidney markers were evaluated in normal Wistar rats over a period of 21 days. Our results show that the rhizome contained 47.12% carbohydrate, 12.87% crude protein, phosphorus, potassium, and calcium. Phytochemical analysis detected phenols, tannins, flavonoids, saponins, glycosides, oxalates, phytates, and trypsin inhibitors. Both extracts lowered plasma glucose levels in a dose‐ and time‐dependent manner. Doses between 200 and 500 mg/kg were well tolerated. Chronic doses ≥ 1000 mg/kg induced hepatotoxicity, marked by elevated AST and ALP levels. High doses of the ethanol extract significantly increased urea levels. We conclude that A. difformis rhizomes possess appreciable nutritional and hypoglycemic properties that support their ethnomedicinal use. However, consumption must be carefully regulated due to dose‐dependent hepatic and renal toxicity during long‐term, high‐dose use.
- Open Access
- 3 January 2026
- Published by Springer Nature in Pflügers Archiv - European Journal of Physiology
- Vol. 478 (1) , 16
Activation of the alternative complement pathway and its relevance for sodium retention in experimental nephrotic syndrome
The complement component C3, factor B (FB) and factor D (FD) belong to the alternative complement pathway and have been identified in urine samples from nephrotic mice. However, it is not yet known whether these factors are involved in mediating sodium retention in nephrotic syndrome (NS). Here we used a genetic mouse model of NS based on an inducible podocin deletion ( Nphs2 Δipod ). These mice were intercrossed with mice deficient for FB, FD or C3, yielding Nphs2 Δipod *Cfb −/− , Nphs2 Δipod *Cfd −/− or Nphs2 Δipod *C3 −/− mice, respectively. NS was induced after oral doxycycline treatment for 14 days. C3, FB and FD were detected in the nephrotic urine of Nphs2 Δipod mice as well as fragments of C3 and FB, indicating intrarenal activation of the alternative complement pathway. Lack of FB and FD had no impact on the activation of C3. Immunohistochemistry demonstrated positive C3 staining in protein casts and within the proximal tubule. Nephrotic mice of all genotypes experienced similar proteolytic activation of the epithelial sodium channel ENaC, developed sodium retention (urinary sodium concentration < 20 mM) and body weight gain. This was associated with a stimulation of proteolytic processing of epithelial sodium channel ENaC in all genotypes. In conclusion, components of the alternative complement pathway are detectable and activated in nephrotic syndrome. Mice with deletion of C3, FB or FD are not protected from proteolytic ENaC activation and sodium retention in NS.
- 3 January 2026
- Published by Springer Nature in Pflügers Archiv - European Journal of Physiology
- Vol. 478 (1) , 16
Open AccessActivation of the alternative complement pathway and its relevance for sodium retention in experimental nephrotic syndrome
The complement component C3, factor B (FB) and factor D (FD) belong to the alternative complement pathway and have been identified in urine samples from nephrotic mice. However, it is not yet known whether these factors are involved in mediating sodium retention in nephrotic syndrome (NS). Here we used a genetic mouse model of NS based on an inducible podocin deletion ( Nphs2 Δipod ). These mice were intercrossed with mice deficient for FB, FD or C3, yielding Nphs2 Δipod *Cfb −/− , Nphs2 Δipod *Cfd −/− or Nphs2 Δipod *C3 −/− mice, respectively. NS was induced after oral doxycycline treatment for 14 days. C3, FB and FD were detected in the nephrotic urine of Nphs2 Δipod mice as well as fragments of C3 and FB, indicating intrarenal activation of the alternative complement pathway. Lack of FB and FD had no impact on the activation of C3. Immunohistochemistry demonstrated positive C3 staining in protein casts and within the proximal tubule. Nephrotic mice of all genotypes experienced similar proteolytic activation of the epithelial sodium channel ENaC, developed sodium retention (urinary sodium concentration < 20 mM) and body weight gain. This was associated with a stimulation of proteolytic processing of epithelial sodium channel ENaC in all genotypes. In conclusion, components of the alternative complement pathway are detectable and activated in nephrotic syndrome. Mice with deletion of C3, FB or FD are not protected from proteolytic ENaC activation and sodium retention in NS.
- Open Access
- 27 October 2025
- Published by Springer Nature in Scientific Reports
- Vol. 15 (1) , 1-10
Alkaline pH and enhanced catalase activity improve the in vitro bio-remediation of crude-oil polluted soil
Bioremediation effectiveness of crude oil-polluted soil can be monitored via bacterial enzyme activity. In this study, crude oil-polluted and non-polluted soil samples were used to prepare various treatment media, and petroleum hydrocarbon (PHC) degradation was assessed at different incubation periods and pH levels by measuring catalase activity. The stimulatory effects of kenaf-core combined with 95% rhamnolipid on in vitro PHC degradation were compared against bio-stimulation and bioaugmentation treatments. All treatments showed peak catalase activity on the 90th day of incubation. Among bio-augmented treatments, AZ1T6 (Azikoro-1) exhibited the highest catalase activity (20.19 mL KMnO4 g−1h−1), followed by OL1T6 (Ologbo-1) and OT1T6 (Otukpoti-1) (17.66 mL KMnO4 g−1h−1), with BN3T6 (Benin-3) showing the lowest (17.33 mL KMnO4 g−1h−1). In bio-stimulated treatments, media supplemented with kenaf-core and rhamnolipid (T4) demonstrated the highest catalase activity at day 90. All bio-stimulated treatments had significantly higher catalase activity compared to the negative control (T7) (P < 0.05), though their activity was statistically lower than in bio-augmented treatments (P < 0.05). Optimal degradation occurred at pH values between 6.0 and 8.0. The synergistic combination of kenaf-core and 95% rhamnolipid likely enhanced nutrient availability, stimulating indigenous microorganisms and catalase activity, thereby improving bioremediation efficiency beyond what either treatment achieved alone. The enhanced effectiveness observed when combining kenaf-core and rhamnolipid, relative to their separate use, provides evidence for a novel synergistic interaction.
- 27 October 2025
- Published by Springer Nature in Scientific Reports
- Vol. 15 (1) , 1-10
Open AccessAlkaline pH and enhanced catalase activity improve the in vitro bio-remediation of crude-oil polluted soil
Bioremediation effectiveness of crude oil-polluted soil can be monitored via bacterial enzyme activity. In this study, crude oil-polluted and non-polluted soil samples were used to prepare various treatment media, and petroleum hydrocarbon (PHC) degradation was assessed at different incubation periods and pH levels by measuring catalase activity. The stimulatory effects of kenaf-core combined with 95% rhamnolipid on in vitro PHC degradation were compared against bio-stimulation and bioaugmentation treatments. All treatments showed peak catalase activity on the 90th day of incubation. Among bio-augmented treatments, AZ1T6 (Azikoro-1) exhibited the highest catalase activity (20.19 mL KMnO4 g−1h−1), followed by OL1T6 (Ologbo-1) and OT1T6 (Otukpoti-1) (17.66 mL KMnO4 g−1h−1), with BN3T6 (Benin-3) showing the lowest (17.33 mL KMnO4 g−1h−1). In bio-stimulated treatments, media supplemented with kenaf-core and rhamnolipid (T4) demonstrated the highest catalase activity at day 90. All bio-stimulated treatments had significantly higher catalase activity compared to the negative control (T7) (P < 0.05), though their activity was statistically lower than in bio-augmented treatments (P < 0.05). Optimal degradation occurred at pH values between 6.0 and 8.0. The synergistic combination of kenaf-core and 95% rhamnolipid likely enhanced nutrient availability, stimulating indigenous microorganisms and catalase activity, thereby improving bioremediation efficiency beyond what either treatment achieved alone. The enhanced effectiveness observed when combining kenaf-core and rhamnolipid, relative to their separate use, provides evidence for a novel synergistic interaction.
- 25 October 2025
- Published by Wiley in The Journal of Physiology
- Vol. 603 (22) , 7365-7382
Hypomagnesaemia‐associated hypokalaemia requires activation of both ENaC and ROMK
Hypokalaemia is common in hypomagnesaemic patients, but the in vivo mechanisms have not been determined. Along the distal nephron, lower intracellular Mg 2+ has been proposed to release the Mg 2+ ‐mediated inhibition of renal outer medullary K + (ROMK) channels, increasing urinary K + excretion. Higher activity of the epithelial Na + channel (ENaC), which provides the driving force for K + secretion via ROMK, may also be required. We tested the hypothesis that hypomagnesaemia‐induced hypokalaemia is associated with higher activities of both ENaC and ROMK. C57BL/6J mice were fed normal (NL), low Mg 2+ (LM), low Na + (LS) or low Na + /Mg 2+ (LS/LM) diets. Kidneys and blood were harvested for western blotting and measurement of plasma [K + ]. ROMK activity was measured by patch‐clamping of split‐open distal convoluted tubule 2 (DCT2)/connecting tubule (CNT) from mice on NL or LS/LM diets. Plasma [K + ] was significantly lower in mice on LS/LM diet. Compared with mice on NL diet, abundances of cleaved α‐ and γ‐ENaC, which correlate with ENaC activity, were higher in mice on LS diet, and lower in mice on LM diet but not on LS/LM diet, suggesting Na + and Mg 2+ restriction counteract each other. A lower natriuretic response to acute amiloride administration confirmed lower ENaC activity in mice on LM diet. ROMK activity along DCT2/CNT was higher in mice on LS/LM but not on LM diet compared with mice on NL diet. Together, our data suggest that Mg 2+ restriction inhibits ENaC activity, and both higher ENaC activity and disinhibition of ROMK are required for the development of hypokalaemia in the context of hypomagnesaemia. image Key points: In patch‐clamping experiments, lower intracellular Mg 2+ releases the Mg 2+ ‐mediated inhibition of renal outer medullary K + (ROMK) channels, increasing urinary K + excretion, but hypomagnesaemia does not always lead to hypokalaemia in several genetic disorders and animal experiments. Epithelial sodium channel (ENaC)‐mediated Na + entry provides the driving force for K + secretion via ROMK, but how hypomagnesaemia affects ENaC activity remains unknown. We found that ENaC activity is lower following dietary Mg 2+ restriction but is preserved with combined Mg 2+ /Na + restriction, stimulating K + secretion via ROMK. Our findings probably explain why Mg 2+ restriction alone cannot cause hypokalaemia in vivo and provide new insights into the mechanisms of hypomagnesaemia‐induced hypokalaemia.
- 25 October 2025
- Published by Wiley in The Journal of Physiology
- Vol. 603 (22) , 7365-7382
Hypomagnesaemia‐associated hypokalaemia requires activation of both ENaC and ROMK
Hypokalaemia is common in hypomagnesaemic patients, but the in vivo mechanisms have not been determined. Along the distal nephron, lower intracellular Mg 2+ has been proposed to release the Mg 2+ ‐mediated inhibition of renal outer medullary K + (ROMK) channels, increasing urinary K + excretion. Higher activity of the epithelial Na + channel (ENaC), which provides the driving force for K + secretion via ROMK, may also be required. We tested the hypothesis that hypomagnesaemia‐induced hypokalaemia is associated with higher activities of both ENaC and ROMK. C57BL/6J mice were fed normal (NL), low Mg 2+ (LM), low Na + (LS) or low Na + /Mg 2+ (LS/LM) diets. Kidneys and blood were harvested for western blotting and measurement of plasma [K + ]. ROMK activity was measured by patch‐clamping of split‐open distal convoluted tubule 2 (DCT2)/connecting tubule (CNT) from mice on NL or LS/LM diets. Plasma [K + ] was significantly lower in mice on LS/LM diet. Compared with mice on NL diet, abundances of cleaved α‐ and γ‐ENaC, which correlate with ENaC activity, were higher in mice on LS diet, and lower in mice on LM diet but not on LS/LM diet, suggesting Na + and Mg 2+ restriction counteract each other. A lower natriuretic response to acute amiloride administration confirmed lower ENaC activity in mice on LM diet. ROMK activity along DCT2/CNT was higher in mice on LS/LM but not on LM diet compared with mice on NL diet. Together, our data suggest that Mg 2+ restriction inhibits ENaC activity, and both higher ENaC activity and disinhibition of ROMK are required for the development of hypokalaemia in the context of hypomagnesaemia. image Key points: In patch‐clamping experiments, lower intracellular Mg 2+ releases the Mg 2+ ‐mediated inhibition of renal outer medullary K + (ROMK) channels, increasing urinary K + excretion, but hypomagnesaemia does not always lead to hypokalaemia in several genetic disorders and animal experiments. Epithelial sodium channel (ENaC)‐mediated Na + entry provides the driving force for K + secretion via ROMK, but how hypomagnesaemia affects ENaC activity remains unknown. We found that ENaC activity is lower following dietary Mg 2+ restriction but is preserved with combined Mg 2+ /Na + restriction, stimulating K + secretion via ROMK. Our findings probably explain why Mg 2+ restriction alone cannot cause hypokalaemia in vivo and provide new insights into the mechanisms of hypomagnesaemia‐induced hypokalaemia.
- 30 April 2025
- Published by Springer Nature in Food Science and Biotechnology
- Vol. 34 (12) , 2881-2895
Toxicological and antioxidant evaluations of the effects of different drying temperatures of the calyx of Hibiscus sabdariffa in experimental rats
Hibiscus sabdariffa calyx is widely used in traditional medicine and as a food ingredient due to its antioxidant potential. This study investigated the toxicological and antioxidant effects of calyx extracts obtained after drying at four temperatures (− 58 °C, 30 °C, 40 °C, and 50 °C) in Wistar rats. Acute toxicity was assessed following the modified Lorke method (24-h observation), and chronic toxicity was evaluated over 28 days using doses of 250, 500, and 1000 mg/kg, in accordance with OECD guideline 407. Although no signs of acute toxicity or significant alterations in organ weights were observed, the antioxidant markers—GSH, CAT, and SOD—were dose-dependently enhanced, with the most potent activity recorded in extracts dried at 30 °C. These findings suggest that drying at 30 °C preserves key bioactive compounds, thereby maximizing the antioxidant potential of H. sabdariffa calyx. The study provides practical insights for optimizing processing conditions for medicinal and nutraceutical applications.
- 30 April 2025
- Published by Springer Nature in Food Science and Biotechnology
- Vol. 34 (12) , 2881-2895
Toxicological and antioxidant evaluations of the effects of different drying temperatures of the calyx of Hibiscus sabdariffa in experimental rats
Hibiscus sabdariffa calyx is widely used in traditional medicine and as a food ingredient due to its antioxidant potential. This study investigated the toxicological and antioxidant effects of calyx extracts obtained after drying at four temperatures (− 58 °C, 30 °C, 40 °C, and 50 °C) in Wistar rats. Acute toxicity was assessed following the modified Lorke method (24-h observation), and chronic toxicity was evaluated over 28 days using doses of 250, 500, and 1000 mg/kg, in accordance with OECD guideline 407. Although no signs of acute toxicity or significant alterations in organ weights were observed, the antioxidant markers—GSH, CAT, and SOD—were dose-dependently enhanced, with the most potent activity recorded in extracts dried at 30 °C. These findings suggest that drying at 30 °C preserves key bioactive compounds, thereby maximizing the antioxidant potential of H. sabdariffa calyx. The study provides practical insights for optimizing processing conditions for medicinal and nutraceutical applications.
- Open Access
- 7 December 2024
- Published by Elsevier in Phytomedicine Plus
- Vol. 5 (1)
Comparative reducing and carbohydrate enzyme inhibitory activities of the root, leaf, and seed of Picralima nitida
- 7 December 2024
- Published by Elsevier in Phytomedicine Plus
- Vol. 5 (1)
Open AccessComparative reducing and carbohydrate enzyme inhibitory activities of the root, leaf, and seed of Picralima nitida
- Open Access
- 9 August 2024
- Published by Wolters Kluwer Health in Kidney360
- Vol. 5 (9) , 1386-1393
Cullin 3/with No Lysine [K] Kinase/Ste20/SPS-Related Proline Alanine Rich Kinase Signaling: Impact on NaCl Cotransporter Activity in BP Regulation
The sodium chloride cotransporter (NCC) fine-tunes Na+ balance and indirectly affects the homeostasis of other ions including K+, Mg2+, and Ca2+. Owing to its effects on Na+ balance, BP is significantly affected by alterations in NCC activity. Several factors have been reported to influence the expression and activity of NCC. One critical factor is NCC phosphorylation/dephosphorylation that occurs at key serine-threonine amino acid residues of the protein. Phosphorylation, which results in increased NCC activity, is mediated by the with no lysine [K] (WNK)-SPS–related proline alanine rich kinase (SPAK)/OSR1 kinases. NCC activation stimulates reabsorption of Na+, increasing extracellular fluid volume and hence BP. On the other hand, proteasomal degradation of WNK kinases after ubiquitination by the Cullin 3-Kelch-like 3 E3 ubiquitin ligase complex and dephosphorylation pathways oppose WNK-SPAK/OSR1-mediated NCC activation. Components of the Cullin 3/Kelch-like 3–WNK-SPAK/OSR1 regulatory pathway may be targets for novel antihypertensive drugs. In this review, we outline the impact of these regulators on the activity of NCC and the consequent effect on BP.
- 9 August 2024
- Published by Wolters Kluwer Health in Kidney360
- Vol. 5 (9) , 1386-1393
Open AccessCullin 3/with No Lysine [K] Kinase/Ste20/SPS-Related Proline Alanine Rich Kinase Signaling: Impact on NaCl Cotransporter Activity in BP Regulation
The sodium chloride cotransporter (NCC) fine-tunes Na+ balance and indirectly affects the homeostasis of other ions including K+, Mg2+, and Ca2+. Owing to its effects on Na+ balance, BP is significantly affected by alterations in NCC activity. Several factors have been reported to influence the expression and activity of NCC. One critical factor is NCC phosphorylation/dephosphorylation that occurs at key serine-threonine amino acid residues of the protein. Phosphorylation, which results in increased NCC activity, is mediated by the with no lysine [K] (WNK)-SPS–related proline alanine rich kinase (SPAK)/OSR1 kinases. NCC activation stimulates reabsorption of Na+, increasing extracellular fluid volume and hence BP. On the other hand, proteasomal degradation of WNK kinases after ubiquitination by the Cullin 3-Kelch-like 3 E3 ubiquitin ligase complex and dephosphorylation pathways oppose WNK-SPAK/OSR1-mediated NCC activation. Components of the Cullin 3/Kelch-like 3–WNK-SPAK/OSR1 regulatory pathway may be targets for novel antihypertensive drugs. In this review, we outline the impact of these regulators on the activity of NCC and the consequent effect on BP.
- Open Access
- 2 January 2024
- Published by Springer Nature in Scientific Reports
- Vol. 14 (1) , 1-13
Bio-augmentation and bio-stimulation with kenaf core enhanced bacterial enzyme activities during bio-degradation of petroleum hydrocarbon in polluted soil
Indigenous micro-organisms often possess the ability to degrade petroleum hydrocarbon (PHC) in polluted soil. However, this process can be improved by supplementing with nutrients or the addition of more potent microbes. In this study, the ability of kenaf-core to stimulate the PHC degradation capability of microbial isolates from PHC polluted soil samples was evaluated. The standard experimental methods used in this study include: the digestion and analysis of the physico-chemical properties of petroleum hydrocarbon contaminated and non-contaminated soil samples; evaluation of petroleum hydrocarbon biodegradation using bio-augmentation and bio-stimulation (with kenaf-core) treatments; and, determination of soil microbial enzyme activities. Results from this study show that K, Na, total nitrogen, organic carbon, exchangeable cations, and heavy metals were found to be significantly (P < 0.05) higher in the polluted soil than in the non-polluted soil. Also, the polluted samples had pH values ranging from 5.5 to 6.0 while the non-polluted samples had a pH of 7.6. The microbial enzyme activities were comparatively lower in the polluted soils as compared to the non-polluted soil. The percentage degradation in the kenaf-core treated samples (AZ1T2—78.38; BN3T2—70.69; OL1T2—71.06; OT1T2—70.10) were significantly (P < 0.05) higher than those of the untreated (AZ1T1—13.50; BN3T1—12.50; OL1T1—10.55; OT1T1—9.50). The degradation of petroleum hydrocarbon in the bio-augmented and bio-stimulated treatments increased with increasing time of incubation, and were higher than that of the untreated sample. Comparatively, the treatment with a combination of kenaf-core and rhamnolipid exhibited a significantly (P < 0.05) higher degradation rate than that of the treatment with only kenaf core or rhamnolipid. While, the bio-stimulated and bio-augmented treatments had appreciable microbial counts that are higher than that of the untreated. In conclusion, the nutrient-supplement with kenaf-core significantly enhanced microbial growth and activities in the soil, thus improving their ability to biodegrade petroleum hydrocarbons in the polluted soils. Thus, supplementing with Kenaf core to encourage microbiological degradation of petroleum hydrocarbon is recommended.
- 2 January 2024
- Published by Springer Nature in Scientific Reports
- Vol. 14 (1) , 1-13
Open AccessBio-augmentation and bio-stimulation with kenaf core enhanced bacterial enzyme activities during bio-degradation of petroleum hydrocarbon in polluted soil
Indigenous micro-organisms often possess the ability to degrade petroleum hydrocarbon (PHC) in polluted soil. However, this process can be improved by supplementing with nutrients or the addition of more potent microbes. In this study, the ability of kenaf-core to stimulate the PHC degradation capability of microbial isolates from PHC polluted soil samples was evaluated. The standard experimental methods used in this study include: the digestion and analysis of the physico-chemical properties of petroleum hydrocarbon contaminated and non-contaminated soil samples; evaluation of petroleum hydrocarbon biodegradation using bio-augmentation and bio-stimulation (with kenaf-core) treatments; and, determination of soil microbial enzyme activities. Results from this study show that K, Na, total nitrogen, organic carbon, exchangeable cations, and heavy metals were found to be significantly (P < 0.05) higher in the polluted soil than in the non-polluted soil. Also, the polluted samples had pH values ranging from 5.5 to 6.0 while the non-polluted samples had a pH of 7.6. The microbial enzyme activities were comparatively lower in the polluted soils as compared to the non-polluted soil. The percentage degradation in the kenaf-core treated samples (AZ1T2—78.38; BN3T2—70.69; OL1T2—71.06; OT1T2—70.10) were significantly (P < 0.05) higher than those of the untreated (AZ1T1—13.50; BN3T1—12.50; OL1T1—10.55; OT1T1—9.50). The degradation of petroleum hydrocarbon in the bio-augmented and bio-stimulated treatments increased with increasing time of incubation, and were higher than that of the untreated sample. Comparatively, the treatment with a combination of kenaf-core and rhamnolipid exhibited a significantly (P < 0.05) higher degradation rate than that of the treatment with only kenaf core or rhamnolipid. While, the bio-stimulated and bio-augmented treatments had appreciable microbial counts that are higher than that of the untreated. In conclusion, the nutrient-supplement with kenaf-core significantly enhanced microbial growth and activities in the soil, thus improving their ability to biodegrade petroleum hydrocarbons in the polluted soils. Thus, supplementing with Kenaf core to encourage microbiological degradation of petroleum hydrocarbon is recommended.