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A survey of the origin, characteristics and possible re-uses of various agriculture and agro-industrial wastes and wastewaters is given. By-products and effluents often contain substances of high-added value that can be directly recovered or can represent a zero- or low-cost substrate for fermentation processes aimed at producing bio-fuels or bio-molecules of actual or potential commercial interest. At first, focus has been put on the general upgrading criteria and strategies. Then, a number of examples have been reported and examined concerning wastes and wastewaters such as residual agricultural and agro-industrial biomasses, relevant effluents (i.e., slaughterhouse, winery and starch industry wastewaters and whey) and by-products of the olive-oil extraction industry.

Different substances may induce neurological impairment, clinically expressed as peripheral neuropathies, due to damage of the neuronal bodies (neuronopathy) of sensory or motor neurons. Neuronopathies have generally been studied referring to neurons, although other cellular components may also be damaged. Cisplatin (CDDP) is known to be neurotoxic to the neurons of the dorsal root ganglia (DRG). The scarcity of information as to the possible involvement and role played by dorsal root ganglion (DRG) satellite cells in neuronopathies prompted this study using the chronic DRG neuronopathy induced by the repeated administration of CDDP in rats as a model. Eighteen female Wistar rats were treated according to 3 different schedules of CDDP administration (6 rats for each group). Six further animals were used as controls. At the end of the experiment the L4-L5-L6 dorsal root ganglia were examined at the light and electron microscope. Ag-NOR reaction was also examined in 4 further CDDP-treated rats and 4 controls. Pathological changes in satellite cells of animals treated with CDDP were remarkable in the nucleus where heterochromatin clumps were reduced or even completely absent. Morphometric analysis of the area occupied by heterochromatin indicated that this nuclear component decreased in an exposure-time dependent manner. Frequently, nucleolar-like structures became apparent in the nucleus of the rats treated with the higher doses of CDDP. Ag-NOR positive regions in the nuclei of treated rats were increased with respect to the controls. Cytoplasmic changes in DRG satellite cells of CDDP treated rats were limited, being characterized by an increased electron-density of the matrix. In treated rats deep invaginations between satellite cells and the neuronal surface were evident, leading to the formation of vacuoli. The interstitial connective space often showed edematous areas. Our observations demonstrate that in chronic cisplatin neuronopathy, DRG satellite cells are also involved in the pathological changes induced by drug exposure, and that these changes may be interpreted as being mainly reactive.

ln humans, the main dose-limiting side-effect of cisplatin (CDDP) treatment is a peripheral sensory neuropathy secondary to dorsal root ganglion (DRG) neuron involvement. To investigate further for neuronal alterations responsible for CDDP neurotoxicity we undertook the present experimental ultrastructural study, based on observations of 3 different groups of rats (6 animals in each group). Group A rats were treated with 1 mg/kg weekly for 9 weeks: Group B with 2 mglkg weekly for 9 weeks; and group C rats served as untreated controls. At the end of the experiment, rats were perfused with 3% glutaraldehyde and lumbar DRGs were prepared for electron microscopic observations. In CDDP-treated rats somatic, nuclear and. above all, nucleolar size was reduced. Ultrastructurally, the nucleolus was the most affected structure. Nucleolar alterations were quantified morphometrically. Less marked changes were seen in the nucleus and in the RER and Golgi apparatus of the cytoplasm. The number of lysosomes and lipofuscins was greatly increased in CDDP-treated rats. The ultrastructural alterations observed in CDDP rats suggest that CDDP may be neurotoxic due to a reduction in protein synthesis. This assumption would explain why cells such as neurons, which are non replicating, but which have a high rate of protein synthesis, may be the target of the neurotoxic action of CDDP. The lack of an efficient blood/nerve barrier in the DRG explains the involvement of this particular type of neuron.

Cisplatin is a very effective antineoplastic drug. To date its major toxic dose-limiting effect is peripheral neuropathy. Whereas the clinical and neurophysiological features of cisplatin-induced neuropathy are fairly well known, its pathogenesis is still unclear. We treated a group of Wistar rats with low doses of cisplatin for 70 days in order to evaluate the light-microscopic and ultrastructural changes induced by chronic cisplatin administration in the spinal cord, spinal ganglia and peripheral nerves. Although the most striking pathological alterations were observed in the spinal ganglia neurons, initial axonal neuropathy was also demonstrated, whereas the spinal cord neurons were completely normal. Our findings further support the hypotheses that spinal ganglion neurons are the primary target of cisplatin peripheral neurotoxicity and that peripheral nerve damage is secondary to this neuronopathy.