Mitochondrial decline in the ageing old world primate retina: Little evidence for difference between the centre and periphery.

Mitochondrial decline is a key feature of ageing. The retina has more mitochondria than any other tissue and ages rapidly. To understand human retinal ageing it is critical to examine old world primates that have similar visual systems to humans, and do so across central and peripheral regions, as there is evidence for early central decline. Hence, we examine mitochondrial metrics in young and ageing Macaca fascicularis retinae. In spite of reduced ATP with age, primate mitochondrial complex activity did not decline. But mitochondrial membrane potentials were reduced significantly, and concomitantly, mitochondrial membrane permeability increased. The mitochondrial marker Tom20 declined significantly, consistent with reduced mitochondria number, while VDAC, a voltage dependent anion channel and diffusion pore associated with apoptosis increased significantly. In spite of these clear age-related changes, there was almost no evidence for regional differences between the centre and the periphery in these mitochondrial metrics. Primate cones do not die with age, but many showed marked structural decline with vacuous spaces in proximal inner segments normally occupied by endoplasmic reticulum (ER), that regulate mitochondrial autophagy. In many peripheral cones, ER was displaced by the nucleus that transposed across the outer limiting membrane and could become embedded in mitochondrial populations. These data are consistent with significant changes in retinal mitochondria in old world primate ageing but provide little if any evidence that aged central mitochondria suffer more than those in the periphery.

Improved mitochondrial function corrects immunodeficiency and impaired respiration in neonicotinoid exposed bumblebees.

Neonicotinoid pesticides undermine pollinating insects including bumblebees. However, we have previously shown that mitochondrial damage induced by neonicotinoids can be corrected by 670nm light exposure. But we do not know if this protection extends to immunity or what the minimum effective level of 670nm light exposure is necessary for protection. We use whole body bee respiration in vivo as a metric of neonicotinoid damage and assess the amount of light exposure needed to correct it. We reveal that only 1 min of 670nm exposure is sufficient to correct respiratory deficits induced by pesticide and that this also completely repairs damaged immunocompetence measured by haemocyte counts and the antibacterial action of hemolymph. Further, this single 1 min exposure remains effective for 3-6 days. Longer exposures were not more effective. Such data are key for development of protective light strategies that can be delivered by relatively small economic devices placed in hives.