Phosphinothricin (glufosinate), an irreversible inhibitor of glutamine synthetase, causes an inhibition of photosynthesis in C3 (Sinapis alba) and C4 (Zea mays) plants under atmospheric conditions (400 ppm CO2, 21% O2). This photosynthesis inhibition is proceeding slower in C4 leaves. Under non-photorespiratory conditions (1000 ppm CO2, 2% O2) there is no inhibition of photosynthesis. The inhibition of glutamine synthetase by phosphinothricin results in an accumulation of NH4 (+). The NH4 (+)-accumulation is lower in C4 plants than in C3 plants. The inhibition of glutamine synthetase through phosphinothricin in mustard leaves results in a decrease in glutamine, glutamate, aspartate, asparagine, serine, and glycine. In contrast to this, a considerable increase in leucine and valine following phosphinothricin treatment is measured. With the addition of either glutamine, glutamate, aspartate, glycine or serine, photosynthesis inhibition by phosphinothricin can be reduced, although the NH4 (+)-accumulation is greatly increased. This indicates that NH4 (+)-accumulation cannot be the primary cause for photosynthesis inhibition by phosphinothricin. The investigations demonstrate the inhibition of transmination of glyoxylate to glycine in photorespiration through the total lack of amino donors. This could result in a glyoxylate accumulation inhibiting ribulose-1,5-bisphosphate-carboxylase and consequently CO2-fixation.

Phosphinothricin (PPT) causes a rapid inhibition of photosynthesis under atmospheric conditions (400 ppm CO2, 21% O2). However, under conditions (1000 ppm CO2, 2% O2) under which photorespiration cannot occur, there is no or only a very low rate of photosynthesis inhibition by phosphinothricin. Under both conditions, a strong NH4+-accumulation is apparent caused through the inhibition of glutamine synthetase by phosphinothricin. This indicates, that NH4+-accumulation cannot be the primary cause for photosynthesis inhibition by phosphinothricin, but a process in connexion with photorespiration plays a central role. Through the lack of amino donors, the transamination of glyoxylate to glycine in photorespiration cannot take place. PPT causes a great decrease in glutamine, glutamate, aspartate, serine, and glycine. Following addition of these amino acids to PPT, there is a decrease in photosynthesis inhibition by PPT. With the addition of glutamine or glutamate to PPT no decrease in serine and glycine is detected, because the transamination of glyoxylate to glycine in photorespiration can occur.

eine B otanik d er Jo h an n es G u ten b erg -U n iv ersität, D -W -6500 M ainz, B undesrepublik D eutschland Z. N aturforsch. 48c, 3 6 9 -3 7 3 (1993); received D ecem ber 2, 1992 G lufosinate, P hosphinothricin, P h o to resp iratio n , Photosynthesis, R ibulose-l,5-bisphosphate C arboxylase G lufosinate (phosphinothricin) irreversibly blocks the glutam ine synthetase which subse quently gives rise to an accum ulation o f am m onium and to a strong decrease in som e am ino acids, especially glutam ine an d glutam ate.U nder atm ospheric conditions (400 ppm C O ,, 21% 0 2) glufosinate causes a rapid inhibition o f photosynthesis, to o . H ow ever, u n d er n o n -p h o to re sp irato ry conditions (1000 ppm C 0 2, 2% 0 2) only a slight inhibition o f p h otosynthesis occurs w ith glufosinate. Since under b oth c o n d i tions an accum ulation o f am m o n iu m occurs, it is concluded th a t inhibition o f photosynthesis is n o t induced by the higher co n cen tratio n s o f am m onium . The results rath er suggest th a t the absence o f am ino do n o rs in the glycolate p ath w ay leads to a break-dow n o f the tran sa m in a tion reaction o f glyoxylate to glycine. This causes an inhibition o f p h o to resp iratio n and as a fu rth er consequence the in hibition o f p h otosynthesis. T here are tw o hypotheses fo r explaining this phenom enon. O ne o f them supposes th a t th e blockade in the glycolate pathw ay produces a lack o f C alvin cycle interm ediates which subsequently is the cause o f the inhibition o f p h o to synthesis. T he o th er one suggests a direct in h ib itio n o f the rib u lo se-l,5 -b isp h o sp h ate carb o x y lase by the accum ulation o f glyoxylate and P-glycolate.A fter treatm ent with different in term ediates o f the C alvin cycle and p h o to resp iratio n to gether w ith glufosinate no decrease in the in h ib itio n o f photosynthesis could be m easured. This suggests th a t the inh ib itio n o f p h o to sy n th esis is n o t induced by a depletion o f in te r m ediates o f the Calvin cycle.Tests on the effect o f glyoxylate an d P-glycolate on ribulosebisphosphate carboxylase activi ty show ed th a t in crude leaves extracts the enzym e activity can only be inhibited by high c o n centrations o f these substances. H ow ever, in in tac t spinach ch loroplasts the enzyme activity can be blocked by using m uch low er c o n cen tratio n s o f glyoxylate. TThis m ay indicate th a t the ribulosebisphosphate carboxylase activase is affected by this m etabolite and th a t this m ay be the reason for an inhibition o f p h o tosynthesis a fter treatm en t w ith glufosinate.

Based on evidence of an increased rate of respiratory infections in sudden infant death (SID) infants as well as the observation of familial occurrence, we analysed in a retrospective study class II and class II genes of the major histocompatibility complex in 40 cases of SID by Southern blot analysis of DNA obtained post mortem from tissue samples. In 24 cases, the parents were interviewed and confirmatory human lymphocyte antigen (HLA) and DNA typing was carried out. Using HLA-DR beta and -DQ beta probes, no evidence of an abnormal HLA-DR frequency distribution in SID infants was detected (P = 0.97). Using DNA probes for the tandemly arranged complement C4 and steroid 21-hydroxylase genes, an increased number of C4B gene deletions in SID cases was found. The increase in C4 gene deletions was significant (P = 0.0125) in infants with recurrent infections. These data indicate a possible role of partial C4 deficiency as a genetically predisposing risk factor in SID.

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