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James C. Bartholomew

Researcher at University of California, Berkeley

Publications -  44
Citations -  3426

James C. Bartholomew is an academic researcher from University of California, Berkeley. The author has contributed to research in topics: Benzo(a)pyrene & Cell cycle. The author has an hindex of 22, co-authored 44 publications receiving 3328 citations. Previous affiliations of James C. Bartholomew include Lawrence Berkeley National Laboratory.

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Aromatic hydrocarbon responsiveness-receptor agonists generated from indole-3-carbinol in vitro and in vivo: comparisons with 2,3,7,8-tetrachlorodibenzo-p-dioxin.

TL;DR: The aromatic hydrocarbon responsiveness-receptor Kd values are reported and it is shown that indolo[3,2-b]carbazole (ICZ) is produced from I3C in yields on the order of 0.01% in vitro and, after oral intubation, in vivo, and ICZ and related condensation products appear responsible for the enzyme-inducing effects of dietary I2C.
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Molecular analysis of H2O2-induced senescent-like growth arrest in normal human fibroblasts: p53 and Rb control G1 arrest but not cell replication.

TL;DR: H2O2-treated cells show a transient elevation of p53, high level of p21, lack of Rb phosphorylation, G1 arrest and inability to replicate when G1 Arrest is inactivated, as measured by the formation of 8-oxo-2'-deoxyguanosine in DNA.
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Mitochondrial decay in hepatocytes from old rats: Membrane potential declines, heterogeneity and oxidants increase

TL;DR: Mitochondrial function during aging was assessed in isolated rat hepatocytes to avoid the problem of differential lysis when old, fragile mitochondria are isolated, suggesting age-associated alterations in mitochondrial membrane potential, the driving force for ATP synthesis.
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Feeding acetyl-l-carnitine and lipoic acid to old rats significantly improves metabolic function while decreasing oxidative stress

TL;DR: ALCAR+LA partially reversed the age-related decline in average mitochondrial membrane potential and significantly increased hepatocellular O2 consumption, indicating that mitochondrial-supported cellular metabolism was markedly improved by this feeding regimen.
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(R)-α-Lipoic acid-supplemented old rats have improved mitochondrial function, decreased oxidative damage, and increased metabolic rate

TL;DR: (R)‐α‐Lipoic acid‐supplemented old rats have improved mitochondrial function, decreased oxidative damage, and increased metabolic rate, which improves indices of metabolic activity as well as lowers oxidative stress and damage evident in aging.