Browsing by Author "Amuji, Doris Nnenna"

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Corrigendum to “Phytochemical composition, acute and subacute toxicity profile of Persea amaricana seed oil in albino Wistar rats” [Toxicol. Rep. 14 (2025) 101982]
(Toxicology Reports (Elsevier), 2025) Iweala, Emeka J.; Okore, Finian Uchenna; Okoro, Benedict Chukwuebuka; Dania, Omoremime Elizabeth; Amuji, Doris Nnenna; Ugbogu, Eziuche A.
GC–MS analysis of locally processed palm kernel oil and its mild ameliorative effects on carbon tetrachloride-induced toxicity in rats
(Comparative Clinical Pathology, 2025-11) Ugbogu, Eziuche A.; Iweala, Emeka J.; Jessie‑Green, Gina; Amuji, Doris Nnenna; Nwankwo, Nnamdi; Okoro, Benedict Chukwuebuka; Dania, Omoremime Elizabeth
This study investigated the phytochemical composition of locally processed palm kernel oil (LPPKO) and its ameliorative effect on carbon tetrachloride ( CCl4) toxicity in albino Wistar rats. Phytochemical composition was analysed by gas chromatography–mass spectrometry (GC–MS). For acute toxicity, a single oral dose of up to 5000 mg/kg LPPKO was administered. On day 1, groups 2–5 experimental rats received a single dose of 1 mL/kg CCl4 diluted 1:1 in olive oil. Thirty minutes after CCl4 administration, rats in groups 3, 4, and 5 received LPPKO orally at 100, 200, and 300 mg/kg body weight, respectively, for 14 days. GC–MS analysis identified nine bioactive compounds with pharmacological properties, including 9,12-octadecadienoic acid (Z,Z) and β-sitosterol. The acute toxicity assessment revealed no detectable signs of toxicity or mortality. The results showed a significant (P < 0.05) increase in high-density lipoproteins, superoxide dismutase (SOD), glutathione (GSH), and catalase (CAT) and a significant (P < 0.05) decrease in aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), urea, total cholesterol, platelets, chloride, and malondialdehyde (MDA) in the LPPKO-treated groups compared to the CCl4- induced untreated groups (negative control) in both male and female rats. LPPKO treatment has a positive effect on CCl4- induced toxicity in rats by decreasing ALT, AST, ALP, and MDA and increasing SOD, GSH, and CAT. This study shows that LPPKO has the potential to mildly reduce the toxic effect of CCl4 on the liver of Wistar rats.
Phytochemical composition, acute and subacute toxicity profile of Persea amaricana seed oil in albino Wistar rats
(Toxicology Reports, 2025) Iweala, Emeka Joshua; Okore, Finian Uchenna; Okoro, Benedict Chukwuebuka; Dania, Omoremime Elizabeth; Amuji, Doris Nnenna; Ugbogu, Eziuche Amadike
Objective: This study investigated the phytochemical composition and toxicity profile of Persea americana seed oil (PASO) in albino Wistar rats. Methods: Chromatography-mass spectrometry (GC-MS) was used to analyse the chemical constituents of PASO. For the acute toxicity test, PASO was administered orally in a single dose of up to 3000 mg/kg body weight (bw). For the subacute toxicity test, the rats were divided into four (4) groups. Group I (normal control), while groups II, III and IV received 200, 300 and 400 mg/kg PASO daily, respectively, for 14 days. Results: In the acute toxicity test, the lethal dose (LD50) of PASO was estimated to be 1477.83 mg/kg. In the subacute toxicity test, PASO significantly increased (p < 0.05) aspartate aminotransferase, creatine phosphokinase, alanine aminotransferase, creatinine, alkaline phosphatase, urea, malondialdehyde, high density lipoprotein, interleukin 1-beta (IL-1β), tumour necrosis factor (TNF-α) and cardiac troponin and significantly decreased glutathione, red blood cells (RBC), packed cell volume (PCV), superoxide dismutase and catalase compared to the control group. Conclusion: Our study showed that the LD50 of PASO is 1477.83 mg/kg body weight, which classifies it as a moderately toxic substance. In subacute toxicity, our results revealed that treatment with PASO resulted in an increase in liver enzymes, urea and creatinine, and inflammatory markers, and a decrease in antioxidant enzymes, suggesting that PASO impairs liver and kidney functions and may cause cardiac or muscle damage in albino Wistar rats.
Protein biomarkers for diagnosis of breast cancer
(Scientific African, 2024) Iweala, Emeka Joshua; Amuji, Doris Nnenna; Nnaji, Faith Chinasaokwu
Breast cancer remains a major global health challenge, demanding better diagnostic tools. Traditional methods like mammography have limitations, highlighting the need for specific, noninvasive approaches. Protein biomarkers offer a promising avenue for early and accurate detection, potentially leading to improved patient outcomes and personalized treatment. This review explores key protein biomarkers, including Estrogen Receptor (ER), Progesterone Receptor (PR), Human Epidermal Growth Factor Receptor 2 (HER-2), and Cancer Antigen 27.29(CA27.29), focusing on the proteomic methodologies used in their discovery and validation. However, challenges exist, such as variability in biomarker expression and limitations in abundance, stability, and specificity, which hinder clinical use. The review discusses innovative strategies to overcome these challenges, emphasizing the importance of translating biomarker research into practical applications for personalized medicine in breast cancer diagnosis and therapy. This exploration contributes to the evolving field of breast cancer diagnostics, paving the way for future discoveries and improved patient care.
Targeting c-Met in breast cancer: From mechanisms of chemoresistance to novel therapeutic strategies
(Current Research in Pharmacology and Drug Discovery, 2024) Iweala, Emeka Eze Joshua; Amuji, Doris Nnenna; Oluwajembola, Abimbola Mary; Ugbogu, Eziuche Amadike
Breast cancer presents a significant challenge due to its heterogeneity and propensity for developing chemo resistance, particularly in the triple-negative subtype. c-Mesenchymal epithelial transition factor (c-Met), a re ceptor tyrosine kinase, presents a promising target for breast cancer therapy due to its involvement in disease progression and poor prognosis. However, the heterogeneous expression of c-Met within breast cancer subtypes and individual tumors complicates targeted therapy. Also, cancer cells can develop resistance to c-Met inhibitors through various mechanisms, including bypass signaling pathways and genetic mutations. The off-target effects of c-Met inhibitors further limit their clinical utility, necessitating the development of more selective agents. To overcome these challenges, personalized treatment approaches and combination therapies are being explored to improve treatment efficacy while minimizing adverse effects. Novel c-Met inhibitors with improved selectivity and reduced off-target toxicity show promise in preclinical studies. Additionally, targeted delivery systems aim to enhance drug localization and reduce systemic toxicity. Future directions involve refining inhibitor design and integrating c-Met inhibition into personalized treatment regimens guided by molecular profiling. This review explores the mechanisms by which c-Met contributes to chemoresistance in breast cancer and current challenges in targeting c-Met for breast cancer therapy. It discusses strategies to optimize treatment outcomes, ultimately improving patient prognosis and reducing mortality rates associated with this devastating disease
Unraveling the potential of USP8 as a therapeutic target for overcoming c-Met-mediated resistance in breast cancer: A review
(Cancer Treatment and Research Communications, 2026) Amuji, Doris Nnenna; Zakari, Suleiman; Pirisola, Ayomikun Joshua; Ogunlana, Olubanke Olujoke; Iweala, Emeka E.J.
Therapeutic resistance remains a serious challenge in breast cancer, and abnormal c-mesenchymal epithelial transition factor (c-Met) receptor tyrosine kinase (RTK) activation contributes to therapeutic resistance in many. Ubiquitin-specific peptidase 8 (USP8) has emerged as a modulator of RTK stability through deubiquitination and endosomal trafficking, and preclinical studies show that inhibition of USP8 speeds up ubiquitin-dependent degradation of RTKs, including c-Met and EGFR, suppresses PI3K/Akt and MAPK signaling, and reverses resis tance phenotypes. In this review, we summarize mechanistic evidence for USP8 regulation of c-Met and related RTKs, explore preclinical studies that assess inhibition of USP8 as a strategy to sensitize RTK-driven tumors, and highlight translational limitations such as drug selectivity, toxicity, dosing, pharmacodynamics biomarkers, and patient selection that must be addressed prior to a clinical trial in breast cancer. While the therapeutic targeting of USP8 is promising, direct validation in breast cancer models and the development of robust pharmacodynamic markers and inhibitors that are clinically graded remain crucial next phase