We have demonstrated that seizures induced by kainic acid (KA) are, at least in part, mediated via oxidative stress in rats [Life. Sci. 61 (1997) PL373; Brain Res. 853 (2000) 215; Brain Res. 874 (2000) 15; Neurosci. Lett. 281 (2000) 65]. In order to extend our findings, we employed the rodent aging model in this study. After KA treatments (once a day for 5 days; 20,20,20,20 and 40 mg/kg, i.p.), several parameters reflecting neurotoxic behaviors, oxidative stress [malondialdehyde (MDA) and protein carbonyl] and aging (lipofuscin-like substances) were compared between senile-prone (P8) and resistant (R1) strains of 9-month-old male senescence-accelerated mice (SAM). KA-induced neurotoxic signs as shown by mortality and seizure activity were more accentuated in the SAM-P8 than in the SAM-R1. Levels of MDA and carbonyl are consistently higher in the hippocampus of SAM-P8 than that of SAM-R1. Significant increases in the values of MDA and carbonyl were observed 4 h or 2 days after the final KA administration. This finding was more pronounced in the SAM-P8 than in the SAM-R1. Although a significant loss of hippocampal neurons was observed 7 days post-KA, at this time the MDA and carbonyl content had returned to near control levels. In contrast, fluorescent lipofuscin-like substances and lipofuscin granules were significantly increased 7 days after KA treatments. Therefore, our data suggests that mice in the senescence model are more susceptible to KA-induced seizures/oxidative damage, and that oxidative damage could be one of the casual factors in the accumulation of lipofuscin.
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http://dx.doi.org/10.1016/s0166-4328(01)00382-5 | DOI Listing |
ASN Neuro
January 2024
Department of Clinical Medicine, University of Bergen, Bergen, Norway.
Elevated levels of Chitinase-3-like protein-1 (CHI3L1) in cerebrospinal fluid have previously been linked to inflammatory activity and disease progression in multiple sclerosis (MS) patients. This study aimed to investigate the presence of CHI3L1 in the brains of MS patients and in the cuprizone model in mice (CPZ), a model of toxic/metabolic demyelination and remyelination in different brain areas. In MS gray matter (GM), CHI3L1 was detected primarily in astrocytes and in a subset of pyramidal neurons.
View Article and Find Full Text PDFJ Food Sci
April 2023
School of Food and Biological Engineering, Hefei University of Technology, Hefei, China.
To evaluate infrared radiation (IR) blanching in comparison to conventional hot water (HW) blanching in inhibiting the browning and extending the shelf life of pecan kernels, the technology of IR blanching at 500-700 W for 90-45 s or HW blanching at 90°C for 60 s, and subsequently drying with hot air at 60, 70, and 80°C, respectively, was used, and then the activities of lipoxidase (LOX) and polyphenol oxidase (PPO), antioxidant capacities, color change, microscopic structure, and the shelf life of kernels were analyzed. Results showed that IR blanching not only significantly decreased the subsequent drying time but also effectively inactivated the activities of LOX and PPO, showing a lower residual activity of 15.74%-40.
View Article and Find Full Text PDFJ Biophotonics
May 2023
Clinical Biobank Center, Microbiome Medicine Center, Department of Laboratory Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
The 3D visualization based on tissue clearing technology allows us to have a deeper understanding of the 3D spatial information of deep molecules in the tissue. Tissue clearing and bacterial labeling methods have been used for in situ 3D microbiota imaging, and we have developed a pipeline for 3D visualization of in situ microbiota in human gliomas. Anti-LPS antibodies are appropriate to label and characterize bacteria in situ within tumors.
View Article and Find Full Text PDFOphthalmic Genet
February 2022
Centre for Ophthalmology and Visual Science (Incorporating Lions Eye Institute), the University of Western Australia, Nedlands, Western Australia, Australia.
Background: Stargardt disease (STGD1) is an autosomal recessive retinal dystrophy due to mutations in ABCA4, characterized by subretinal deposition of lipofuscin-like substances and bilateral centrifugal vision loss. Despite the tremendous progress made in the understanding of STGD1, there are no approved treatments to date. This review examines the challenges in the development of an effective STGD1 therapy.
View Article and Find Full Text PDFClin Exp Ophthalmol
July 2021
Centre for Ophthalmology and Visual Science (Incorporating Lions Eye Institute), The University of Western Australia, Nedlands, Western Australia, Australia.
Stargardt disease (STGD1) is an autosomal recessive retinal dystrophy, characterised by bilateral progressive central vision loss and subretinal deposition of lipofuscin-like substances. Recent advances in molecular diagnosis and therapeutic options are complemented by the increasing recognition of new multimodal imaging biomarkers that may predict genotype and disease progression. Unique non-invasive imaging features of STDG1 are useful for gene variant interpretation and may even provide insight into the underlying molecular pathophysiology.
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