Phycocyanin moderates aging and proteotoxicity in Caenorhabditis elegans

Singh, Niraj Kumar; Sonani, Ravi R.; Awasthi, Anjali; Prasad, Birendra; Patel, Anjali R.; Kumar, Jitendra; Madamwar, Datta

doi:10.1007/s10811-015-0772-5

Cited by 22 publications

(13 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Treatment of transgenic nematodes producing a Q40 protein with the antioxidants Vitamin C, α-lipoic acid and epigallocatechin failed to ameliorate movement defects and polyQ aggregation [ 185 ]. However, when the same nematode model was treated with the antioxidant phycocyanin the number of polyQ aggregates was reduced, suggesting that all antioxidants are not equally effective [ 186 ]. Several other antioxidants were reported to have beneficial effects in nematode HD models.…”

Section: Pharmacological Strategies Against Polyq Diseasesmentioning

confidence: 99%

Oxidative Stress and Neurodegeneration: Interconnected Processes in PolyQ Diseases

et al. 2021

View full text Add to dashboard Cite

Neurodegenerative polyglutamine (polyQ) disorders are caused by trinucleotide repeat expansions within the coding region of disease-causing genes. PolyQ-expanded proteins undergo conformational changes leading to the formation of protein inclusions which are associated with selective neuronal degeneration. Several lines of evidence indicate that these mutant proteins are associated with oxidative stress, proteasome impairment and microglia activation. These events may correlate with the induction of inflammation in the nervous system and disease progression. Here, we review the effect of polyQ-induced oxidative stress in cellular and animal models of polyQ diseases. Furthermore, we discuss the interplay between oxidative stress, neurodegeneration and neuroinflammation using as an example the well-known neuroinflammatory disease, Multiple Sclerosis. Finally, we review some of the pharmaceutical interventions which may delay the onset and progression of polyQ disorders by targeting disease-associated mechanisms.

show abstract

Section: Pharmacological Strategies Against Polyq Diseasesmentioning

confidence: 99%

Oxidative Stress and Neurodegeneration: Interconnected Processes in PolyQ Diseases

et al. 2021

View full text Add to dashboard Cite

show abstract

“…R42DM 33 Leptolyngbya sp. N62DM 31 Phormidium sp. A09DM 9 In vitro (Biochemical assay)DPPH assay (% DPPH scavenging)63.15 ± 0.8571.10 ± 0.0674.85 ± 2.14%72.26 ± 1.21%FRAP assay (Ascorbic acid equivalent antioxidant Capacity)0.22 ± 0.010.29 ± 0.050.49 ± 0.040.46 ± 0.06Reducing power assay (Ascorbic acid equivalent antioxidant Capacity)0.40 ± 0.010.44 ± 0.030.53 ± 0.050.48 ± 0.04 In vivo ( C. elegans )DCFH-DA staining (% reduction in fluorescence intensity)88.7078.8883.11Not availableProtective effect against oxidative stress (Fraction survival in %)84.04 ± 6.2780.00 ± 7.0767.2 ± 6.4064.9 ± 5.10Protective effect against thermal stress (Increase in fraction survival in %)~36~10~25Not available…”

Section: Resultsmentioning

confidence: 99%

“…Antioxidant assays, 2,2-diphenyl-1-picrylhydrazyl (DPPH)-radical scavenging activity, ferric ion reducing ability of plasma (FRAP) and reducing power (RP) assay were performed as described earlier 31 . The in - vivo antioxidant activity was assessed using C .…”

Section: Methodsmentioning

confidence: 99%

Phylogenetic and crystallographic analysis of Nostoc phycocyanin having blue-shifted spectral properties

Sonani

Rastogi

Patel

et al. 2019

Sci Rep

Self Cite

View full text Add to dashboard Cite

The distinct sequence feature and spectral blue-shift (~10 nm) of phycocyanin, isolated from Nostoc sp. R76DM (N-PC), were investigated by phylogenetic and crystallographic analyses. Twelve conserved substitutions in N-PC sequence were found distributed unequally among α- and β-subunit (3 in α- and 9 in β-subunit). The phylogenetic analysis suggested that molecular evolution of α- and β-subunit of Nostoc -phycocyanin is faster than evolution of Nostoc -species. The divergence events seem to have occurred more frequently in β-subunit, compared to α-subunit (relative divergence, 7.38 for α-subunit and 9.66 for β-subunit). Crystal structure of N-PC was solved at 2.35 Å resolution to reasonable R-factors (R work /R Free = 0.199/0.248). Substitutions congregate near interface of two αβ-monomer in N-PC trimer and are of compensatory nature. Six of the substitutions in β-subunit may be involved in maintaining topology of β-subunit, one in inter-monomer interaction and one in interaction with linker-protein. The β153Cys-attached chromophore adopts high-energy conformational state resulting due to reduced coplanarity of B- and C-pyrrole rings. Distortion in chromophore conformation can result in blue-shift in N-PC spectral properties. N-PC showed significant in - vitro and in - vivo antioxidant activity comparable with other phycocyanin. Since Nostoc -species constitute a distinct phylogenetic clade, the present structure would provide a better template to build a model for phycocyanins of these species.

show abstract

“…Singh et al assayed phycocyanin, an antioxidant protein from phycobiliproteins plants [ 128 ], in worms expressing 40Q in muscle cells (AM141) [ 120 ]. In contrast with the study by Machiela et al, phycocyanin significantly reduced the number of inclusion bodies in these animals [ 120 ]. These apparent conflicting results, and the results reported for EGCG, show the complexity of using drugs that may be pleiotropic.…”

Section: Oxidative Stress and Huntington Diseasementioning

confidence: 99%

Reactive Species in Huntington Disease: Are They Really the Radicals You Want to Catch?

et al. 2020

View full text Add to dashboard Cite

Huntington disease (HD) is a neurodegenerative condition and one of the so-called rare or minority diseases, due to its low prevalence (affecting 1–10 of every 100,000 people in western countries). The causative gene, HTT, encodes huntingtin, a protein with a yet unknown function. Mutant huntingtin causes a range of phenotypes, including oxidative stress and the activation of microglia and astrocytes, which leads to chronic inflammation of the brain. Although substantial efforts have been made to find a cure for HD, there is currently no medical intervention able to stop or even delay progression of the disease. Among the many targets of therapeutic intervention, oxidative stress and inflammation have been extensively studied and some clinical trials have been promoted to target them. In the present work, we review the basic research on oxidative stress in HD and the strategies used to fight it. Many of the strategies to reduce the phenotypes associated with oxidative stress have produced positive results, yet no substantial functional recovery has been observed in animal models or patients with the disease. We discuss possible explanations for this and suggest potential ways to overcome it.

show abstract

Phycocyanin moderates aging and proteotoxicity in Caenorhabditis elegans

Cited by 22 publications

References 50 publications

Oxidative Stress and Neurodegeneration: Interconnected Processes in PolyQ Diseases

Oxidative Stress and Neurodegeneration: Interconnected Processes in PolyQ Diseases

Phylogenetic and crystallographic analysis of Nostoc phycocyanin having blue-shifted spectral properties

Reactive Species in Huntington Disease: Are They Really the Radicals You Want to Catch?

Contact Info

Product

Resources

About