Lipopolysaccharide-induced platinum accumulation in the cerebral cortex after cisplatin administration in mice: Involvement of free radicals

Minami, Takeshi; Okazaki, Jiro; Kawabata, Atsufumi; Kawaki, Hideko; Okazaki, Yuko

doi:10.1016/s1382-6689(96)00064-6

Cited by 13 publications

(4 citation statements)

References 22 publications

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“…Indeed, the idea that chemotherapy accumulates in the human brain has been debated, and likely depends on the type of chemotherapy, the dose density, and other factors that may compromise the blood brain barrier (Branca et al, 2018). In rodents, although paclitaxel has been found in the brain after peripheral infusions (Cavaletti et al, 2000), cisplatin has only been found in the brain under extreme circumstances such as excessive chemotherapy dose (Screnci, McKeage et al, 2000), hypoxia, or lipopolysaccharide challenge (Minami et al, 1996a;Minami et al, 1996b;Minami et al, 1996c;Minami et al, 1998). There is relatively more evidence that the spinal cord accumulates neurotoxic chemotherapy, such as oxaliplatin found in the cerebrospinal fluid (Huang et al, 2016) and DRG in humans (Krarup-Hansen et al, 1999) and rodents (Screnci et al, 2000), perhaps because the DRG lack the protective blood brain barrier.…”

Section: Overall Discussionmentioning

confidence: 99%

Review of the Role of the Brain in Chemotherapy-Induced Peripheral Neuropathy

Omran

Belcher

Mohile

et al. 2021

Front. Mol. Biosci.

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Chemotherapy-induced peripheral neuropathy (CIPN) is a common, debilitating, and dose-limiting side effect of many chemotherapy regimens yet has limited treatments due to incomplete knowledge of its pathophysiology. Research on the pathophysiology of CIPN has focused on peripheral nerves because CIPN symptoms are felt in the hands and feet. However, better understanding the role of the brain in CIPN may accelerate understanding, diagnosing, and treating CIPN. The goals of this review are to (1) investigate the role of the brain in CIPN, and (2) use this knowledge to inform future research and treatment of CIPN. We identified 16 papers using brain interventions in animal models of CIPN and five papers using brain imaging in humans or monkeys with CIPN. These studies suggest that CIPN is partly caused by (1) brain hyperactivity, (2) reduced GABAergic inhibition, (3) neuroinflammation, and (4) overactivation of GPCR/MAPK pathways. These four features were observed in several brain regions including the thalamus, periaqueductal gray, anterior cingulate cortex, somatosensory cortex, and insula. We discuss how to leverage this knowledge for future preclinical research, clinical research, and brain-based treatments for CIPN.

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Section: Overall Discussionmentioning

confidence: 99%

Review of the Role of the Brain in Chemotherapy-Induced Peripheral Neuropathy

Omran

Belcher

Mohile

et al. 2021

Front. Mol. Biosci.

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“…5 Besides, CP is also known to generate reactive oxygen species (ROS) and reactive nitrogen species (RNS) upon accumulating in the target cells that can alter the normal physiological redox status of the cells resulting into such deleterious effects, including the drug-induced neurotoxicity. 6,7 Riboflavin (RF) or vitamin B 2 is an essential vitamin occurring in all forms of life. It participates in various enzymecatalyzed metabolic redox reactions in the forms of FAD and FMN.…”

Section: Introductionmentioning

confidence: 99%

Cisplatin-Induced NeurotoxicityIn VivoCan Be Alleviated by Riboflavin Under Photoillumination

Hassan

Chibber²,

Khan³

et al. 2013

Cancer Biotherapy and Radiopharmaceuticals

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Cisplatin (CP)-induced neurotoxicity is one of the major clinical problems in CP-based chemoradiotherapy, leading to its discontinuation depending upon their severity. In the present investigation, the photosensitizing property of riboflavin (RF) has been used to ameliorate the CP-induced neurotoxicity. According to dosing plan, the healthy mice were given RF, CP, and their combinations under photoillumination with their controls without any light exposure. After the treatment, antioxidant enzymes, cellular reductants, glutathione-S-transferase, brain markers, and oxidation products were assessed besides histopathology in their brain samples. These parameters revealed that RF ameliorates CP-induced neurotoxicity in a dose-dependent manner under photoillumination. Hence, inclusion of RF in CP-based chemoradiotherapy can be an effective strategy to counter CP-induced neurotoxicity.

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“…Cisplatin contains a platinum group which forms covalent adducts with bases in DNA, resulting in the apoptotic death of cancer cells, as well as other rapidly dividing cells [3]. Cisplatin also results in the activation of a cascade of proinflammatory interleukins [4], causes nitrosative and oxidative stress [5,6], and activates p53 protein which induces apoptosis [3,7,8]. Although cisplatin is an effective anticancer agent, it causes liver and kidney toxicities, as well as testicular toxicity and ototoxicity [9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Nano Ellagic Acid Counteracts Cisplatin-Induced Upregulation in OAT1 and OAT3: A Possible Nephroprotection Mechanism

et al. 2020

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Cisplatin is an anticancer drug commonly used for solid tumors. However, it causes nephrotoxicity. OAT1 and OAT3 are organic anion transporters known to contribute to the uptake of cisplatin into renal tubular cells. The present study was designed to examine the protective role of ellagic acid nanoformulation (ellagic acid nano) on cisplatin-induced nephrotoxicity in rats, and the role of OAT1/OAT3 in this effect. Four groups of male Wistar rats were used (n = 6): (1) control, (2) cisplatin (7.5 mg/kg single dose, intraperitoneal), (3) cisplatin + ellagic acid nano (1 mg/kg), and (4) cisplatin + ellagic acid nano (2 mg/kg). Nephrotoxic rats treated with ellagic acid nano exhibited a significant reduction in elevated serum creatinine, urea, and oxidative stress marker, malondialdehyde (MDA). Additionally, ellagic acid nano restored renal glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). Ellagic acid nano improved the histopathological changes induced by cisplatin, such as tubular dilatation, necrosis, and degeneration. Interestingly, OAT1 and OAT3 showed significantly lower expression at both mRNA and protein levels following ellagic acid nano treatment relative to the cisplatin-exposed group. These findings reveal a potential inhibitory role of ellagic acid antioxidant on OAT1 and OAT3 expression and thus explains its nephroprotective effect against cisplatin nephrotoxicity.

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Lipopolysaccharide-induced platinum accumulation in the cerebral cortex after cisplatin administration in mice: Involvement of free radicals

Cited by 13 publications

References 22 publications

Review of the Role of the Brain in Chemotherapy-Induced Peripheral Neuropathy

Review of the Role of the Brain in Chemotherapy-Induced Peripheral Neuropathy

Cisplatin-Induced NeurotoxicityIn VivoCan Be Alleviated by Riboflavin Under Photoillumination

Nano Ellagic Acid Counteracts Cisplatin-Induced Upregulation in OAT1 and OAT3: A Possible Nephroprotection Mechanism

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