Chronic green tea consumption prevents age-related changes in rat hippocampal formation.

Neurobiol Aging. 2009 May 1.

Assunção M, Santos-Marques MJ, Carvalho F, Lukoyanov NV, Andrade JP.
Department of Anatomy, Faculty of Medicine, University of Porto, Alameda Prof. Hernâni Monteiro, 4200-319 Porto, Portugal.

The hippocampal formation undergoes considerable structural and functional modifications during aging and oxidative stress emerges as a key player in the process. In the present study, we investigated whether prolonged consumption of green tea (GT), which contains large amounts of polyphenols, could interfere with age-related changes in this brain region using biochemical, morphological and behavioral approaches. Ten male Wistar rats aged 19 months were fed with GT since 12 months of age and results compared to those obtained from controls aged 19 months (C-19M). At 12 months of age, another group of rats was evaluated to provide baseline data. Oxidative stress markers (protein carbonyls and malondialdehyde) were quantified in hippocampal homogenates and stereological methods were applied to estimate the deposition of lipofuscin in hippocampal CA3 pyramidal neurons. Morris water maze was used to assess spatial learning and memory. Aging increased oxidative markers and lipofuscin accumulation and was associated with impaired memory acquisition. However, GT treatment protected proteins and lipids against oxidation and prevented the increase of lipofuscin deposition compared to age-matched controls. Furthermore, the spatial learning abilities of GT-treated rats were significantly improved when compared to those from C-19M group. Taken together, these findings confirm the neuroprotective ability of GT in the hippocampal formation probably due to the reduction of oxidative stress-related damage observed during aging.

PMID: 19411127

I’m pretty sure this has been covered before, but nonetheless, here’s their abstract. I don’t have access to this journal, Planta Medica, unfortunately, so I can’t tell if it had any effect on maximum lifespan, but since it wasn’t reported in the abstract I assume it didn’t.

Epigallocatechin Gallate from Green Tea (Camellia sinensis) Increases Lifespan and Stress Resistance in Caenorhabditis elegans.

Planta Med. 2008 Dec 11; PMID: 19085685

Abbas S, Wink M.

Institute of Pharmacy and Molecular Biotechnology, University of Heidelberg, Heidelberg, Germany.

Epigallocatechin gallate (EGCG) is a major green tea polyphenol with pronounced antioxidative activity. The effects of EGCG on lifespan and stress resistance in wild-type N2 and transgenic strains of CAENORHABDITIS ELEGANS [ HSP-16.2/GFP, MEV-1(KN1), FEM-1(HC17)] were investigated. The expression of HSP-16.2 (induced by the pro-oxidant juglone) and the intracellular levels of H (2)O (2) were inhibited by EGCG treatment. Daily administration of 220 muM EGCG increased the mean lifespan by 10.14 % and 14.27 % in N2 and FEM-1(HC17) strains, respectively, and 55 muM EGCG increased the mean lifespan in MEV-1(KN1) by 16.11 %. The survival rate was also increased under lethal oxidative stress by 65.05 %. These findings suggest that the increased mean lifespan and stress resistance in C. ELEGANS apparently depend, among other factors, on the antioxidant properties of EGCG.

Significant longevity-extending effects of EGCG on Caenorhabditis elegans under stress.

Free Radic Biol Med. 2008 Nov 5; PMID: 19061950

Zhang L, Jie G, Zhang J, Zhao B.

Epigallocatechin gallate (EGCG), a main active ingredient of green tea, is believed to be beneficial in association with anticarcinogenesis, antiobesity, and blood pressure reduction. Here we report that EGCG extended Caenorhabditis elegans longevity under stress. Under heat stress (35 degrees C), EGCG improved the mean longevity by 13.1% at 0.1 mug/ml, 8.0% at 1.0 mug/ml, and 11.8% at 10.0 mug/ml. Under oxidative stress, EGCG could improve the mean longevity of C. elegans by 172.9% at 0.1 mug/ml, 177.7% at 1.0 mug/ml, and 88.5% at 10.0 mug/ml. However, EGCG could not extend the life span of C. elegans under normal culture conditions. Further studies demonstrated that the significant longevity-extending effects of EGCG on C. elegans could be attributed to its in vitro and in vivo free radical-scavenging effects and its up-regulating effects on stress-resistance-related proteins, including superoxide dismutase-3 (SOD-3) and heat shock protein-16.2 (HSP-16.2), in mutant C. elegans with SOD-3Colon, two colonsgreen fluorescent protein (GFP) and HSP-16.2Colon, two colonsGFP expression. Quantitative real-time PCR results showed that the up-regulation of aging-associated genes such as daf-16, sod-3, and skn-1 could also contribute to the stress resistance attributed to EGCG. As the death rate of a population is closely related to the mortality caused by external stress, it could be concluded that the survival-enhancing effects of EGCG on C. elegans under stress are very important for antiaging research.