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Cytodex 1 microcarriers have been used for the successful culture of more than 80 different types of animal cells--including primary cells, normal diploid cell strains and established or transformed cell lines. culture volumes have ranged from a few milliliters for diagnostic studies to over several hundred liters for vaccine production. Experience with this wide variety of cell types and culture volumes has enabled the identification of several parameters critical for obtaining maximum cell yields from microcarrier cultures. The most vital stage for the successful microcarrier culture of many cell types was the initial stage of the culture cycle. To achieve high cell yields, it was necessary to use culture procedures which maximized plating efficiency and final cell yield could be further increased by ensuring that the inoculation cell density exceeded a critical viable cell/microcarrier ratio. Modifications of the standard microcarrier culture procedures included reducing initial culture volume, reducing the initial stirring speed and/or supplementing the medium during the early stages of the culture cycle. Control of pH, nutrient supply, and gas tension were all critical throughout the culture cycle. Results with low-serum and serum-free media indicate that the requirement for fetal calf serum in the microcarrier culture of Vero and MRC-5 cells can be reduced or even eliminated. Large scale microcarrier culture equipment should take into account the modified culture procedures which are often required to achieve the full potential of this culture method. The design of a new flexible culture system suitable for pilot and production scale cultures is presented. This system accomodates a wide variety of culture and production procedures and through a recirculation system permits: (a) "in-line" monitoring and control of culture parameters; (b) provides an efficient gas exchange capacity which obviates the need for fermenter headspace and sparging; and (c) allows for maximal utilization of medium components and rapid harvesting of medium or cell products.

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The pesticide DDT was examined for possible mutagenicity in mice, D. melanogaster and N. crassa. Through the use of the dominant-lethal assay it was found that acute oral doses of DDT (2 x 150 mg/kg body weight) in male mice induced dominant lethal mutations in early spermatid and spermatocyte stages. Chronic oral doses of DDT (2 x 100 mg/kg body weight per week for 10 weeks) in male mice caused a persistent increase in the number of dominant lethal mutations. Histological sections showed that chronic treatment of mice with DDT caused changes in seminiferous tubule morphology and degeneration of B-type spermatogonia. Acute treatment of mice with DDT caused an increase in spermatocyte chromosome breakage, stickiness and precocious separation of the X and Y bivalent.Oral treatment of male Canton-S D. melanogaster with DDT caused an increase in dominant lethality in early spermatid and spermatocyte stages. DDT also caused non-disjunction of the X and Y chromosomes at the spermatocyte stage in treated male y/R(1)2,vj/B s yy+ D. melanogaster. The shift in sex ratio is discussed in terms of breakage of the ring-X chromosome. Treatment of a population of Canton-S D. melanogaster with DDT for eight months did not cause any increase in frequency of second-chromosome recessive lethal mutations.In tests for the induction of recessive lethal mutations in the ad-3 region of an N. crassa heterokaryon the results were inconclusive. However, in the host-mediated assay with N. crassa and mice as the host, DDT did not appear to be mutagenic.The results show that DDT has a deleterious effect on reproduction in mice and is a weak mutagen in both mice and D. melanogaster.