Tag: malondialdehyde

Role of Reactive Oxygen Species and Antioxidants in Atopic Dermatitis

This 2013 case-control study by Sivaranjani et al. assessed oxidative stress markers in 25 patients with atopic dermatitis (AD) compared to 25 healthy controls. The study found significantly elevated levels of malondialdehyde (MDA), a marker of lipid peroxidation, in AD patients. Concurrently, there was a marked reduction in both enzymatic

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Serum antioxidative enzymes levels and oxidative stress products in age-related cataract patients

This case-control study assessed oxidative stress and antioxidant enzyme levels in 60 patients with age-related cataracts compared to 60 healthy controls. Results showed significantly reduced serum activities of key antioxidant enzymes—superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px)—in cataract patients. Concurrently, levels of oxidative stress markers such as malondialdehyde

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Role of alpha-lipoic acid in counteracting paclitaxel- and doxorubicin-induced toxicities: a randomized controlled trial in breast cancer patients

This 2022 randomized, double-blind, placebo-controlled trial investigated the effects of alpha-lipoic acid (ALA) in reducing chemotherapy-induced toxicities in 64 women with breast cancer undergoing treatment with doxorubicin, cyclophosphamide, and paclitaxel. Patients were assigned to receive either ALA (600 mg/day) or placebo for six months. ALA significantly improved chemotherapy-induced peripheral neuropathy

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Is Curcumin Intake Really Effective for Chronic Inflammatory Metabolic Disease? A Review of Meta-Analyses of Randomized Controlled Trials

This systematic review analyzed 54 meta-analyses of randomized controlled trials to assess the effectiveness of curcumin supplementation in managing chronic inflammatory metabolic diseases. Curcumin was found to significantly reduce inflammatory markers like CRP, IL-6, and TNF-α; lower oxidative stress (as indicated by decreased MDA); and improve glucose metabolism (reducing FBG,

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A review of recent studies on malondialdehyde as toxic molecule and biological marker of oxidative stress

This systematic review examines malondialdehyde (MDA), a product of polyunsaturated fatty acid peroxidation, highlighting its role as a toxic molecule and a biomarker of oxidative stress. MDA forms adducts with DNA and proteins, contributing to mutagenesis and atherogenesis, with elevated levels observed in oxidative stress-related conditions such as cardiovascular diseases

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Assessment of lipid peroxidation by measuring malondialdehyde (MDA) and relatives in biological samples: Analytical and biological challenges

This systematic review examines the challenges in assessing lipid peroxidation through biomarkers such as malondialdehyde (MDA), 4-hydroxy-nonenal (HNE), and 15(S)-8-iso-prostaglandin F₂α (15(S)-8-iso-PGF₂α), which indicate oxidative stress and cellular damage. These markers originate from both enzymatic and non-enzymatic reactions involving polyunsaturated fatty acids (PUFAs), complicating their accurate quantification. The review highlights

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Neuronal mitochondrial toxicity of malondialdehyde: inhibitory effects on respiratory function and enzyme activities in rat brain mitochondria

This in vitro study investigated the effects of malondialdehyde (MDA), a byproduct of lipid peroxidation, on mitochondrial function in rat brain mitochondria. MDA exposure led to a dose-dependent reduction in mitochondrial membrane potential, inhibited complex I- and II-linked respiration, and suppressed the activity of key enzymes like NADH dehydrogenase, succinate

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The cytotoxic mechanism of malondialdehyde and protective effect of carnosine via protein cross-linking/mitochondrial dysfunction/reactive oxygen species/MAPK pathway in neurons

This in vitro study explored the cytotoxic effects of malondialdehyde (MDA), a product of lipid peroxidation, on cortical neurons and the protective role of carnosine. MDA exposure led to decreased neuronal viability, triggering both apoptosis and necrosis, mediated by reactive oxygen species (ROS) generation, mitochondrial dysfunction, and activation of JNK

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