International journal of biochemistry and molecular biology最新文献

Objectives: Telomere length, the markers of biological aging, can be influenced by risk factors that may lead to health issues like chronic non-communicable diseases. This study explored the paternal telomere length influenced by diseases like diabetes and hypertension with age and its association with newborn telomere length (TL) and the telomerase gene.

Methods: In this cross-sectional study, 204 father-newborn dyads were recruited. The qPCR was used for the quantification of TL (T/S ratio), and Sanger sequencing was done for telomerase (TERT) genotype identification. Statistical Package for Social Sciences (SPSS) and GraphPad Prism Software were used for data analysis. The Spearman correlation was used to find an association between father and newborn TL. The Kruskal-Wallis and Mann-Whitney test was used to find differences among disease groups and TL. The P<0.05 was considered statistically significant.

Results: A positive correlation (r=0.39) (P<0.0001) was seen among fathers and newborn TL. The mean TL (T/S ratio) was found to be longer in healthy fathers and their newborns (1.67±1.18, 2.36±1.39), whereas significantly shorter TL (1.41±0.98, 2.02±1.58) (P=0.000) was seen in fathers suffering from diseases. The healthy fathers and their newborns TL (2.94±0.72, 3.10±0.61) were seen longer in the 15-20 (yrs) age category. Moreover, newborns of fathers (41-45 yrs) with both diabetes and hypertension had significantly longer telomere length (3.20±2.92) compared to their fathers (1.15±1.65) (P=0.006). The TERT risk genotype AC (rs2736100) was the most prevalent among the newborn girls.

Conclusion: A positive association with shorter TL in newborns was found in fathers having chronic diseases such as diabetes and hypertension, highlighting the contribution of fathers in reprogramming newborns' telomere biology.

Background: Paracetamol is a widely used over-the-counter drug for pain relief and fever management. However, its misuse through chronic overuse or acute overdose presents significant risks to human health, primarily causing hepatotoxicity and systemic oxidative stress.

Methodology: This study evaluated the hepatoprotective, antioxidant, and anti-inflammatory effects of aqueous leaf extracts of Celosia trigyna and Euphorbia hirta in mitigating paracetamol-induced liver damage in male Wistar rats.

Results: Paracetamol administration (150 mg/kg) significantly elevated liver function markers (ALT, AST, ALP, and bilirubin), oxidative stress parameters (MDA), and inflammatory cytokines (IL-6 and TNF-α), while depleting antioxidant defenses (SOD and GSH). Disrupted lipid profiles were also observed in the paracetamol-only group. Pretreatment with Celosia trigyna and Euphorbia hirta extracts (125 mg/kg and 250 mg/kg) effectively ameliorated these effects by normalizing liver function markers, reducing oxidative stress and inflammation, and restoring lipid profiles. Molecular docking identified bioactive compounds such as rutin, quercetin, and kaempferol as potent inhibitors of Glutathione-S-Transferase, Tumor Necrosis Factor-alpha, and Cytochrome P450, with binding affinities of -9.3, -7.2, and -8.3 kcal/mol, respectively. These interactions underpin the antioxidant and anti-inflammatory activities observed in vivo.

Conclusion: These findings suggest that Celosia trigyna and Euphorbia hirta have the potential to serve as natural prophylactic or therapeutic agents for mitigating paracetamol toxicity. Further research is required to isolate their active compounds and explore their synergistic potential with conventional treatments. This study bridges traditional medicine and modern pharmacology, offering innovative approaches to managing drug-induced liver.

Edible oils and ghee are vital parts of our daily culinary practices. In recent years, owing to heightened demand in the domestic and global markets, consistent reports regarding the adulteration of edible oils and ghee with substandard ingredients have been reported. Adulteration in edible oils is widespread, with distinctive contaminants, including cottonseed, mineral, and lower-cost oils like palm olein. In the case of ghee, it is repeatedly combined with animal fats, synthetic materials, or vanaspati. The consumption of contaminated oils and trans-fats within the human diet has resulted in adverse health effects, including cardiovascular diseases, digestive disorders, and even cancer. The review aims to summarize various adulterants found in edible oil (mustard oil) and ghee, their detection techniques, and harmful effects. This review provides an overview of the contemplation linked to the adulteration of edible oils and ghee, the compliance with relevant regulations, and the technological approaches available for detection. The detection technologies for identifying adulteration in edible oils are chromatography and spectroscopy biochemical methods and the use of high-precision analytical instruments. The presence of adulterants in edible oil and ghee undermines our societal integrity and our ethical standards. Awareness among consumers is essential for effectively combating these adulterations.

Objective: Lately, various scientists have been paying a lot of consideration to the design of operational antimicrobial agents due to the rise of multiple drug-resistant strains. Therefore, this work is aimed at discovering the biochemical behavior of the analyzed polypeptides in relation to glutamine amidotransferase GatD (pdb id: 5n9m) for gram positive bacteria and beta-lactamase class A (pdb id: 5fqq) for gram negative bacteria. Additionally, this study aims to identify the specific atoms involved in the observed biochemical interactions between the studied complexes using computational methods.

Methods: In this work, five polypeptides were studied using insilico approach via Spartan 14 software, molecular operating environment, ADMETSar, and Gromacs.

Results: The descriptors obtained revealed the activities of the studied compounds, the molecular interaction between the studied ligands as well as glutamine amidotransferase GatD (pdb id: 5n9m) and beta-lactamase class A (pdb id: 5fqq) which thereby exposed compound 1 and 5 to be the compounds with greatest ability to inhibit the studied targets among other studied compounds.

Conclusion: Our discoveries may open door for the design of collection of proficient polypeptide-based drug-like compounds as potential anti-microbial agents.

The family of fibroblast growth factors (FGFs) consists of 22 members with diverse biological functions in cells, from cellular development to metabolism. The family can be further categorized into three subgroups based on their three modes of action. FGF19, FGF21, and FGF23 are endocrine FGFs that act in a hormone-like/endocrine manner to regulate various metabolic activities. However, all three members of the endocrine family require both FGF receptors (FGFRs) and klotho co-receptors to elicit their functions. α-klotho and β-klotho act as scaffolds to bring endocrine FGFs closer to their receptors (FGFRs) to form active complexes. Numerous novel studies about metabolic FGFs' structures, mechanisms, and physiological insights have been published to further understand the complex molecular interactions and physiological activities of endocrine FGFs. Herein, we aim to review the structures, physiological functions, binding mechanisms to cognate receptors, and novel biomedical applications of endocrine FGFs in recent years.

In this paper, we explore marine bioactive peptides with anticancer potential sourced from various marine organisms, including tunicates, sea sponges, and mollusks. Peptides like Stylisin and Papuamides have been isolated, identified, and modified to enhance their activity, with many advancing to clinical trials due to their diverse biological activities, promising prospects in medicine. Enzymatic hydrolysis is a favored method for extracting peptides from marine proteins, particularly from sponges known for their rich bioactive compounds. Compounds such as Jaspamide and Homophymins exhibit potent cytotoxic activity against cancer cells, underscoring their therapeutic potential. Additionally, peptides from ascidians and mollusks, such as Aplidine and Kahalalide F, demonstrate significant anticancer properties. This study also explores peptides influencing apoptosis, microtubule dynamics, and angiogenesis, providing insights into potential mechanisms for cancer treatment. While peptides like Neovastat and mycothiazole target known pathways, others such as patellamides act through unknown mechanisms, highlighting the intricate interactions of marine peptides with cancer cells. Overall, marine-derived peptides show promise as valuable candidates for developing novel anticancer therapies.

Marine environments harbor a wealth of bioactive peptides with potential anticancer properties, sourced from diverse organisms like tunicates, sea sponges, and mollusks. Through isolation, identification, and modification, peptides such as Stylisin and Papuamides have shown enhanced activity and progressed to clinical trials, underscoring their therapeutic promise. Enzymatic hydrolysis emerges as a favored method for peptide extraction from marine proteins, with sponges identified as particularly rich sources. Compounds like Jaspamide and Homophymins exhibit potent cytotoxic activity against cancer cells, highlighting their therapeutic potential. Additionally, peptides from ascidians and mollusks, including Aplidine and Kahalalide F, demonstrate significant anticancer properties. The study delves into peptides affecting apoptosis, microtubule dynamics, and angiogenesis inhibition, offering insights into potential cancer treatment mechanisms. Marine-derived peptides hold great promise as valuable candidates for novel anticancer therapies, with ongoing research aimed at unlocking their full therapeutic benefits.

Cadmium (Cd) is a heavy metal pollutant widely distributed in the environment due to industrial activities, mining, and agricultural practices. Cadmium-induced Toxicity exerts profound effects on ER functioning through multiple mechanisms, leading to cellular dysfunction and pathological consequences. Cadmium disrupts protein folding and activates the unfolded protein response (UPR). Cd exposure leads to the accumulation of misfolded proteins, triggering UPR pathways mediated by critical ER transmembrane sensors: IRE1, PERK, and ATF6. The subsequent UPR aims to restore ER homeostasis but can also induce apoptosis under severe stress conditions. Cd disrupts ER calcium homeostasis by inhibiting the SERCA pump, further exacerbating ER stress. The generation of reactive oxygen species (ROS also plays a critical role in Cd toxicity, damaging ER-resident proteins and amplifying UPR activation). Cadmium also affects the lipid metabolism. This review examines the mechanisms by which Cd toxicity impairs ER functioning, disruption of protein folding and quality control mechanisms, and dysregulation of calcium signaling and lipid metabolism. The subsequent cellular consequences, including oxidative stress, apoptosis, and inflammation, are discussed in the context of Cd-induced pathogenesis of diseases such as Cancer and neurodegenerative and cardiovascular disorders. Finally, potential therapeutic strategies must be explored to mitigate the adverse effects of Cd on ER functioning and human health.

Objectives: The current study aimed to correlate OCT1 (organic cation transporter 1) polymorphisms with metformin response variability in Iraqi women with PCOS (polycystic ovarian syndrome) and determine the impact of OCT1 polymorphism. PCOS, an endocrine metabolic disorder, can seriously impact female health including infertility. Although its cause is unclear, it is usually known to be associated with hormonal imbalances. OCT1 is essential for metformin absorption in the liver. Recent research shown that OCT1 polymorphisms affects metformin responsiveness.

Methods: In the present work, a prospective case-control study was conducted at Department of Infertility, Karbala Teaching Hospital for Obstetrics and Gynecology. 100 PCOS patients and 50 healthy controls aged 20-40 were enrolled. Consultant gynecologist diagnosed PCOS patients using Rotterdam criteria and recommended metformin 500 mg twice daily for 3 months. At the start of the trial and after 3 months, all patients and healthy controls underwent hormonal, biochemical and genetic tests.

Results: The similar allelic frequencies of OCT1 polymorphism in PCOS and control groups was observed. Most patients with reference wild type alleles (C) showed considerable hormonal and metabolic responses to metformin, while those with mutant alleles (T) showed non-significant responses.

Conclusion: FSH, prolactin and testosterone hormonal levels may be considered as candidate biomarkers for PCOS detection and metformin related biomedical respond.

Introduction: Human epidemiological studies have shown that diets rich in plant polyphenols have beneficial effects on various diseases including cancer. Epigallocatechin Gallate, a flavonoid polyphenol molecule, has been shown to be both chemotherapeutic and chemo-preventive in the treatment of several forms of cancer, including lung cancer. 80% of cancers of the lungs are non-small cell lung cancers.

Objective: The study was carried out to see the effects of Epigallocatechin Gallate in non-small cell lung cancer cells (A549) using in-vitro studies.

Materials and methods: Cell Viability Assay was performed using MTT (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) assay. Wound Healing assay was also performed at different concentrations of the compound. Dexamethasone and Doxorubicin, the drugs with anti-cancer properties served as control. A549 cell lines were used.

Results: In the current study, it was demonstrated using Cell viability assay and Wound Healing assay that Epigallocatechin gallate exhibits anti-proliferative activity on A549 lung cancer cells and inhibits cancer cell proliferation in a concentration and time-dependent manner. It was observed that Epigallocatechin gallate (P = 0.0016, P = 0.0018) could significantly inhibit the growth of lung cancer cells with IC50 values 60.55 ± 1.0 μM. The result of wound Healing assay suggests that Epigallocatechin gallate can inhibit the proliferation and migration of A549 cells with concentrations near or higher to 50 μM.

Conclusion: Epigallocatechin gallate's protective effect has been shown in A549 lung adenocarcinoma cells in a time and dose-dependent manner. This suggests the implication of Epigallocatechin gallate for the prevention and therapy for lung cancer.