The chloroplast development in maize (Zea mays L.) is retarded at low growth temperatures. The composition of thylakoid membranes isolated from fiiliy-expanded leaves of plants grown at 17/14 or 14/12 “C (day/night) differed markedly from that of 25/22 "C-grown plants dne to a deficiency of chloroplast-encoded gene products. Appreciable net synthesis of thylakoid proteins in vivo was observed in a 3-h labelling period with p^SJ-methionine at 14/12 “C, but the ratio of accumuiated chloroplast- to nuclear-encoded products was lesser than at 25/22 °C. The protein synthesis by chloroplasts in vitro demonstrated that the accumulation of thylakoid membrane proteins was markedly temperature-dependent. Both the protein assembly into thylakoids and its subsequent breakdown took plače more rapidly at higher temperatures. Extensive differences in nuclear protein composition were observed between maize leaves grown at 14/12 and 25/22 "C, suggesting a possible role for nuclear factors in suppressing the expression of genes for chloroplast proteins at temperatures which inhibit thylakoid assembly.
Perinatal hypoxic-ischemic insult (HII) is one of the main devastating causes of morbidity and mortality in newborns. HII induces brain injury which evolves to neurological sequelae later in life. Hypothermia is the only therapeutic approach available capable of diminishing brain impairment after HII. Finding a novel therapeutic method to reduce the severity of brain injury and its consequences is critical in neonatology. The present paper aimed to evaluate the effect of sulforaphane (SFN) pre-treatment on glucose metabolism, neurodegeneration, and functional outcome at the acute, sub-acute, and sub-chronic time intervals in the experimental model of perinatal hypoxic-ischemic insult in rats. To estimate the effect of SFN on brain glucose uptake we have performed 18F-deoxyglucose (FDG) μCT/PET. The activity of FDG was determined in the hippocampus and sensorimotor cortex. Neurodegeneration was assessed by histological analysis of Nissl-stained brain sections. To investigate functional outcomes a battery of behavioral tests was employed. We have shown that although SFN possesses a protective effect on glucose uptake in the ischemic hippocampus 24 h and 1 week after HII, no effect has been observed in the motor cortex. We have further shown that the ischemic hippocampal formation tends to be thinner in HIE and SFN treatment tends to reverse this pattern. We have observed subtle chronic movement deficit after HII detected by ladder rung walking test with no protective effect of SFN. SFN should be thus considered as a potent neuroprotective drug with the capability to interfere with pathophysiological processes triggered by perinatal hypoxicischemic insult.