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.

Melatonin protects the mitochondria from oxidative damage reducing oxygen consumption, membrane potential, and superoxide anion production.

J Pineal Res. 2008 Nov 19; PMID: 19054298
Lopez A, Garcia JA, Escames G, Venegas C, Ortiz F, Lopez LC, Acuna-Castroviejo D.

Centro de Investigacion Biomedica, Parque Tecnologico de Ciencias de la Salud, Universidad de Granada, Granada, Spain.

The role of melatonin in improving mitochondrial respiratory chain activity and increasing ATP production in different experimental conditions has been widely reported. To date, however, the mechanism(s) involved are largely unknown. Using high-resolution respirometry, fluorometry and spectrophotometry we studied the effects of melatonin on normal mitochondrial functions. Mitochondria were recovered from mouse liver cells and incubated in vitro with melatonin at concentrations ranging from 1 nm to 1 mm. Melatonin decreased oxygen consumption concomitantly with its concentration, inhibited any increase in oxygen flux in the presence of an excess of ADP, reduced the membrane potential, and consequently inhibited the production of superoxide anion and hydrogen peroxide. At the same time it maintained the efficiency of oxidative phosphorylation and ATP synthesis while increasing the activity of the respiratory complexes (mainly complexes I, III, and IV). The effects of melatonin appeared to be due to its presence within the mitochondria, since kinetic experiments clearly showed its incorporation into these organelles. Our results support the hypothesis that melatonin, together with hormones such as triiodothyronine, participates in the physiological regulation of mitochondrial homeostasis.