Microcystin-RR (MCRR), a very widespread toxic microcystin in China, has previously been proved to induce sensitive apoptosis in Carassius auratus lymphocytes in vitro. This study focused on the role of intracellular Ca(2+), mitochondrial membrane potential, reactive oxygen species, and intracellular ATP in the mechanism of MCRR-induced apoptotic toxicity to fish lymphocytes. Compared with controls, administration of MCRR (10 nmol L(-1)) caused a massive calcium influx resulting in elevation of reactive oxygen species (ROS), rapid disruption of mitochondrial membrane potential (DeltaPsim), and depletion of ATP. This study provided a possible mechanism for the cytotoxicity of microcystins to fish lymphocytes.

Microcystin-LR (MCLR), the most toxic microcystin up to date, could induce apoptosis in many kinds of fish and mammalian cells. For the fish immunotoxicity, it was found that MCLR could induce apoptosis in Carassius auratus lymphocytes in vitro. So this study focused on the role of intracellular Ca(2+), mitochondrial membrane potential, reactive oxygen species (ROS), and intracellular ATP in response to the mechanisms of MCLR-induced apoptosis in fish lymphocytes. MCLR (10 nM) administration resulted in a massive elevation in ROS, intracellular Ca(2+), decreased ATP, and rapid mitochondrial membrane potential (DeltaPsi(m)) disruption. When compared to controls, both a fourfold significant (P < 0.001) elevation in O(2) (-) in 1.5 h and an approximately twofold increase in Ca(2+) in 0.5 h were observed. After 6 h of treatment, an approximately 30% decrease for DeltaPsi(m) but about 75% decline for ATP were found. Together, the results demonstrated that MCLR-induced apoptosis was associated with a massive calcium influx, resulting in O(2) (-) elevation, DeltaPsi(m) disruption, and ATP depletion. This study provided a possible cytotoxic mechanism of fish lymphocytes caused by MCLR.

Miscanthus is one of the most promising bioenergy crops with high photosynthetic nitrogen-use efficiency (PNUE). It is unclear how nitrogen (N) influences the photosynthesis in Miscanthus. Among three Miscanthus genotypes, the net photosynthetic rate (P N ) under the different light intensity and CO 2 concentration was measured at three levels of N: 0, 100, and 200 kg ha -1 . The concentrations of chlorophyll, soluble protein, phosphoenolpyruvate carboxylase (PEPC), ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco) large subunit, leaf anatomy and carbon isotope discrimination (Δ) in the leaf were analyzed to probe the response of photosynthesis in Miscanthus genotypes to N levels. P N in all genotypes rose significantly as N application increased. The initial slope of response curves of P N to C i was promoted by N application in all genotypes. Both stomatal conductance and C i were increased with increased N supply, indicating that stomatal factors played an important role in increasing P N . At a given C i , P N in all genotypes was enhanced by N, implying that nonstomatal factors might also play an important role in increasing P N . Miscanthus markedly regulated N investment into PEPC rather than the Rubisco large subunit under higher N conditions. Bundle sheath leakiness of CO 2 was constant at about 0.35 for all N levels. Therefore, N enhanced the photosynthesis of Miscanthus mainly by increasing stomatal conductance and PEPC concentration.

To investigate how bisulfite promotes photosynthesis, a pot experiment was conducted with rice (Oryza sativa L.) plants to determine Rubisco activity and content, and Rubisco activase (RCA) gene expression after spraying NaHSO 3 on rice leaves. The NaHSO 3 treatment promoted significantly net photosynthetic rate (P N ), carboxylation efficiency, maximum carboxylation rate, ribulose-1,5-bisphosphate regeneration rate, initial Rubisco activity, and RCA protein and mRNA concentrations. Therefore, the NaHSO 3 enhancement of P N could be directly attributed to induction of RCA gene expression both at the transcription and translation levels. Thus, the increased RCA regulated the initial Rubisco activity in vivo.

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