Dinuclear [(TPyA)M-II(CA(2-))M-II(TPyA)](2+) [TPyA = tris(2-pyridylmethyl)amine; CA(2-) = chloranilate dianion; M = Co (1(2+)), Fe (2(2+))] complexes have been prepared by the reaction of M(BF4)(2)center dot 6H(2)O, TPyA, H(2)CA, and triethylamine in MeOH solution. Their reduced forms [(TPyA)M-II(CA(center dot 3-))M-II(TPyA)](+) [M = Co(1(+)), Fe (2(+))] have been synthesized by using cobaltocene, and oxidized forms of 1, [(TPyA)Co-III(CA(n))Co-III(TPyA)](z+) [z = 3, n = 3- (1(3+)); z = 4, n = 2- (1(4+))], have been obtained by using FcBF(4) and ThianBF(4) (Fc = ferrocenium; Thian = thianthrinium), respectively. The dinuclear compound bridged chloranilates (CA(2-) or CA(center dot 3-)) were isolated and characterized by X-ray crystallography, electrochemistry, magnetism, and EPR spectroscopy. Unlike the other redox products, valence ambiguous 1(3+) forms via a complex redox-induced valence electron rearrangement whereby the one-electron oxidation of the [Co(II)CA(2-)Co(II)](2+) core forms [Co(III)CA(center dot 3-)Co(III)](3+), not the expected simple 1-e(-) transfer mixed-valent [Co(II)CA(2-)Co(III)](3+) core. The M ions in 1 and 2 have a distorted octahedral geometry by coordination with four nitrogens of a TPyA, two oxygens of a chloranilate. Due to the interdimer offset face-to-face pi-pi and/or herringbone interactions, all complexes show extended 1-D and/or 2-D supramolecular structures. The existence of CA(center dot 3-) in 1(3+) is confirmed from both solid-state magnetic and solution EPR data. Co-based 1(n+) exhibit antiferromagnetic interactions [1(2+): g = 2.24, J/k(B) = -0.65 K (-0.45 cm(-1)); 1(+): g = 2.36, J/k(B) = -75 K (52 cm(-1))], while Fe-based 2(n+) exhibit ferromagnetic interactions [2(2+): g = 2.08, J/k(B) = 1.0 K (0.70 cm(-1)); 2(+): g = 2.03, J/k(B) = 28 K (19 cm(-1))] [H = -2JS(1)center dot S-2 for 1(2+) and 2(2+); H = -2J(S-1 center dot S-2 + S-2 center dot S-3) for 1(+) and 2(+)]. Thus, due to direct spin exchange CA(center dot 3-) is a much strong spin coupling linkage than the superexchange spin-coupling pathway provided by CA(2-).